Application of STK26 gene in preparation of medicine for treating or preventing osteoporosis

Abstract

The invention belongs to the technical field of biological medicines, discloses application of an STK26 gene in preparation of medicines for treating or preventing osteoporosis, and particularly relates to application of STK26 protein or a coding gene thereof in preparation of medicines for treating osteoporosis. According to the present invention, osteoclast differentiation is inhibited by knocking out the STK26 gene so as to treat osteoporosis, osteoclast differentiation can be promoted by overexpressing the specific STK26 protein and the encoded gene thereof so as to aggravate osteoporosis, and osteoporosis can be alleviated by specifically knocking out the STK26 in an ovariectomized osteoporosis mouse model and an age-related osteoporosis mouse model; overexpression of the STK26 recombinant protein can aggravate osteoporosis, and the STK26 protein and the coding gene thereof can be used as targets of clinical drug treatment, and have good prospects in screening and preparation of drugs for treating osteoporosis.

Description

Technical Field

[0001] This invention belongs to the field of biomedical technology, specifically relating to the application of the STK26 gene in the preparation of drugs for the treatment or prevention of osteoporosis. Background Technology

[0002] Osteoporosis is a systemic bone disease caused by various factors, resulting in decreased bone density and quality, destruction of bone microstructure, and increased bone fragility, making patients prone to fractures. Currently, medications used to treat osteoporosis can be mainly divided into estrogen preparations, bisphosphonates, and parathyroid hormone preparations. Long-term use of estrogen preparations may increase the incidence of breast cancer, endometrial cancer, and cardiovascular disease. Bisphosphonates are prone to causing gastrointestinal irritation, and approximately 60% of bisphosphonates entering the bloodstream are excreted unchanged through the kidneys; therefore, they should be used with caution in patients with abnormal renal function. Parathyroid hormone preparations generally refer to teriparatide. Although the treatment effect is very good, patients can only receive a single 24-month treatment in their lifetime. This is because teriparatide has a parathyroid hormone (PTH)-like effect in the body. When the level of PTH in the body is too high, it will overactivate osteoclast activity, leading to severe bone loss and thus worsening osteoporosis.

[0003] Serine / threonine kinase 26 (STK26), also known as Stellile 20-like kinase 4 (MST4), was identified in 2001. Composed of 416 amino acid residues with a relative molecular mass of 46 kDa, it is located on Xq26 and belongs to the GCK-III family of germinal center kinases. It is an important multifunctional protein kinase involved in cytoskeleton rearrangement, morphogenesis, cell proliferation, transformation, and apoptosis. Due to its kinase activity, the biological role of STK26 in various diseases, especially tumor-related diseases, has attracted a surge of research from scholars both domestically and internationally. Domestic scholars have indicated that STK26 could serve as a novel therapeutic target for autophagy and radiosensitivity in gastric cancer. Furthermore, international studies have shown that STK26 can serve as a potential oncogene and therapeutic target for breast cancer. These domestic and international studies demonstrate that STK26 plays a significant biological role in the human body, and a deeper understanding of the relationship between STK26 and disease development is of significant clinical importance. However, the role and mechanism of STK26 in osteoporosis have not yet been reported domestically or internationally.

[0004] TRAF proteins are signal transducer molecules, and all six members (TRAF1-6) have been identified and can bind to different amino acid sites on RANK. However, it appears that only TRAF6-deficient mice exhibit severe osteopetrosis due to impaired osteoclast development, indicating that TRAF6 is essential for functional osteoclast formation in vivo. Furthermore, recent studies have reported that TRAF6-mediated signaling pathways play a crucial role in osteoclast-related diseases such as osteoporosis, further demonstrating the vital regulatory role of TRAF6 in osteoclast formation. The serine / threonine kinase STK26 has two catalytic domains; when activated by signal transduction molecules, STK26 protein can phosphorylate substrate proteins.

[0005] Studies have shown that STK26 maintains a dynamic homeostasis in macrophages through direct phosphorylation and regulation of TRAF6 autoubiquitination activity. Current research on the functional mechanisms of STK26 primarily focuses on tumor-related diseases, and the specific mechanisms by which this key susceptibility gene participates in the progression of osteoporosis have not yet been reported. Therefore, developing novel osteoporosis treatment strategies targeting STK26 holds great promise for innovation and clinical application.

[0006] Based on this, the study investigates and involves the application of the STK26 gene in the preparation of drugs for the treatment or prevention of osteoporosis. Summary of the Invention

[0007] Based on the aforementioned deficiencies in the existing technology, the purpose of this invention is to provide the application of the STK26 (MST4) gene in the preparation of drugs for the treatment or prevention of osteoporosis. Knocking out the STK26 gene can treat or prevent osteoporosis and has shown good bone protection effects in OVX mice and age-related osteoporosis mouse models, providing strong evidence for its application in the preparation or prevention of osteoporosis drugs.

[0008] This invention is achieved through the following technical solution: Application of STK26 gene in the preparation of drugs for the treatment or prevention of osteoporosis, and application of STK26 protein or its encoding gene in the preparation of drugs for the treatment of osteoporosis.

[0009] Furthermore, the amino acid sequence of the STK26 protein is shown in SEQ ID No. 1, and the coding gene sequence of the STK26 protein is shown in SEQ ID No. 2. Furthermore, when preparing drugs for treating osteoporosis using STK26 protein, administration is carried out via intravenous infusion or tail vein injection.

[0010] Furthermore, when preparing drugs for treating osteoporosis using the STK26 protein encoding gene, the STK26 protein encoding gene is specifically knocked out in osteoclasts for drug delivery.

[0011] Furthermore, when preparing drugs for treating osteoporosis using the STK26 protein encoding gene, the STK26 protein encoding gene is introduced into osteoclasts via a lentiviral vector.

[0012] Furthermore, the STK26 protein or its encoding gene can be used as a target for clinical drug therapy.

[0013] The present invention also provides a pharmaceutical composition for treating or preventing osteoporosis, wherein the active substance of the pharmaceutical composition is STK26 protein and its encoding gene.

[0014] Furthermore, when the active substance of the pharmaceutical composition is STK26 protein, it is administered via tail vein injection or intravenous infusion; when the active substance is the encoding gene of STK26 protein, it is administered by overexpressing or knocking out the encoding gene of STK26 protein in osteoclasts.

[0015] This invention also provides the application of the STK26 gene in regulating osteoclast function, wherein the regulation of osteoclast function is the regulation of changes in bone metabolism.

[0016] This invention also provides a method for regulating osteoclast differentiation, which involves knocking out the STK26 gene and using a modified lentivirus to carry the STK26 gene and target it to osteoclasts, thereby knocking out the STK26 gene in osteoclasts and reducing osteoclast differentiation.

[0017] Compared with the prior art, the beneficial effects of the present invention are: 1) The technical solution described in this application treats osteoporosis by knocking out the STK26 gene to inhibit osteoclast differentiation. Overexpression of specific STK26 protein and its encoded gene can promote osteoclast differentiation and aggravate osteoporosis. Furthermore, specific knockout of STK26 in ovariectomized osteoporosis mouse models and age-related osteoporosis mouse models can alleviate osteoporosis, while overexpression of recombinant STK26 protein can aggravate osteoporosis.

[0018] 2) The STK26 protein and its encoding gene in the technical solution of this application have good bone protection effect in the preparation of drugs for treating osteoporosis. Therefore, the STK26 protein and its encoding gene can be used as a target for clinical drug treatment and have good prospects in screening and preparing drugs for treating osteoporosis. Attached Figure Description

[0019] Figure 1This study investigated the upregulation of serine / threonine kinase 26 (STK26), also known as Sterile20-like kinase 4 (MST4), in peripheral blood mononuclear cells from patients with clinical osteoporosis. (A) Detection of MST4 mRNA levels in peripheral blood mononuclear cells from osteoporosis patients and healthy controls using quantitative real-time polymerase chain reaction (RT-qPCR); (BC) Western blot analysis of MST4 protein expression levels in osteoporosis patients and healthy controls, with corresponding statistical results (n = 6); (D) Bone mineral density (BMD) levels in osteoporosis patients and healthy controls; (EF) Expression levels of bone formation markers osteocalcin (OC) and type I procollagen N-terminal propeptide (P1NP) in osteoporosis patients and healthy controls; (GH) Expression levels of bone formation markers β-collagen degradation products (β-CTX) and acid phosphatase 5b (TRAcP). 5b) Expression levels in patients with osteoporosis and healthy controls; (I) Receiver operating characteristic (ROC) curve analysis of MST4 expression for predicting fragility fractures in patients with osteoporosis; * This indicates that the p-value between the two groups is <0.05, and the sample size of each group is n=60; Figure 2 Correlation between STK26 (also known as MST4) expression and serum bone mineral density and bone metabolism markers in osteoporosis patients; (A) Correlation analysis between MST4 mRNA expression level and bone mineral density (BMD); (BC) Correlation analysis between MST4 mRNA expression level and bone formation markers osteocalcin (OC) and type I procollagen N-terminal propeptide (P1NP) expression levels; (DE) Correlation analysis between MST4 mRNA expression level and bone resorption markers β-collagen degradation products (β-CTX) and tartrate-resistant acid phosphatase 5b (TRAcP 5b) expression. * This indicates that the p-value between the two groups is less than 0.05, and the sample size is n=60; Figure 3 Establishment of a mouse ovariectomy (OVX) model and changes in STK26 (MST4) protein expression; (A) Flowchart of animal experiments; (B) Macroscopic morphology and weight of the uterus in the control group, ovariectomy group, ovariectomy + sh- MST4 group, and ovariectomy + oe- MST4 group; (C) Western blot analysis of MST4 protein expression in the tibial tissue of mice in each group, and expression of bone metabolism markers c-Fos, activated T cell nuclear factor 1 (NFATc1), and tartrate-resistant acid phosphatase (TRAP) proteins; * To indicate differences between groups (P<0.05), 6 mice were in each group; Figure 4In vivo safety assessment results of STK26 (MST4) knockdown and overexpression; (A) Blood cell count analysis (white blood cells (WBC), red blood cells (RBC) and platelets (PLT)) before sacrifice at 8 weeks of age: Ovariectomy (OVX) + sh-NC + oe-NC (OVX) group and OVX + sh-MST4 + oe-NC (OVX + sh-MST4) group; (B) Serum biochemical parameters analysis (albumin, amylase, alkaline phosphatase, blood urea nitrogen, calcium, creatinine, globulin, glucose, potassium, sodium, phosphorus, total bilirubin and total protein) before sacrifice at 8 weeks of age: OVX + sh-NC + oe-NC (OVX) group and OVX + sh-MST4 + oe-NC (OVX + sh-MST4) group, each group containing six mice; Figure 5 The results of the effect of STK26 (MST4) on ovariectomy-induced bone loss are shown in the figure; (A) Representative micro-computed tomography (microCT) images of the femur of mice in each group; (B) MicroCT analysis of bone mineral density (BMD), trabecular bone number (Tb.N), thickness (Tb.Th), and separation (Tb.Sp) of mice in each group; (C) Representative images of the femur of mice in each group after hematoxylin-eosin staining, with a scale bar of 200 micrometers; (DE) Representative images of the femur of mice in each group after tartrate-fast acid phosphatase staining, and histomorphometry analysis of osteocyte number (N.Oc / BS per bone surface area) and osteocyte surface area (Oc.S / BS per bone surface area), with a scale bar of 50 micrometers; (F) The maximum load-bearing capacity and stiffness of the femur were determined by the three-point bending test. * The difference between the two groups was statistically significant (P<0.05), with 6 mice in each group; Figure 6Establishment of an age-related osteoporosis model and the effect of STK26 (MST4) on age-related bone loss: (A) Flowchart of animal experiment workflow; (B) Western blot analysis of MST4 and osteoclast metabolic markers (c-Fos, NFATc1, TRAP) in mouse tibia; (C) Representative micro-computed tomography (Micro-CT) images of femur in each group; (D) Micro-CT analysis of bone mineral density (BMD), trabecular bone number (Tb.N), trabecular bone thickness (Tb.Th), and trabecular bone separation (Tb.Sp) in each group; (E) Representative hematoxylin-eosin (H&E) stained images of femur, scale bar = 200 μm; (FG) Representative tartrate-resistant acid phosphatase (TRAP) stained images of femur, including histomorphometric analysis of osteoclast number per unit bone surface (N.Oc / BS) and osteoclast surface area per unit bone surface (Oc.S / BS), scale bar = 50 μm. μm; (H) Results of three-point bending test of femoral maximum load and stiffness, * indicates significant difference between groups (P<0.05), n=6 for each group. Detailed Implementation

[0020] To make the objectives, technical solutions, and advantages of this invention clearer, the invention will be further described in detail below with reference to the embodiments. The illustrative embodiments and descriptions of this invention are only used to explain this invention and are not intended to limit this invention.

[0021] This invention provides the application of the STK26 gene in the preparation of drugs for the treatment or prevention of osteoporosis, specifically the application of the STK26 protein or its encoding gene in the preparation of drugs for the treatment of osteoporosis.

[0022] In this invention, the amino acid sequence of the STK26 protein is shown in SEQ ID No. 1, and the coding gene sequence of the STK26 protein is shown in SEQ ID No. 2. The NCB1 reference sequence of the STK26 gene in this application is NP057626.2; therefore, SEQ ID No. 1 and SEQ ID No. 2 are both prior art.

[0023] In this invention, STK26 protein is used to prepare a drug for treating or preventing osteoporosis, which is administered via intravenous infusion or tail vein injection.

[0024] In the invention, when preparing a drug for treating osteoporosis by specifically knocking out the gene encoding the STK26 protein in osteoclasts, the drug is administered.

[0025] In the invention, when preparing a drug for treating osteoporosis using the STK26 protein encoding gene, the STK26 protein encoding gene is introduced into osteoclasts via a lentiviral vector.

[0026] In this invention, the STK26 protein or its encoding gene is used as a target for clinical drug therapy.

[0027] The present invention also provides a pharmaceutical composition for treating osteoporosis, wherein the active substance of the pharmaceutical composition is STK26 protein and its encoding gene.

[0028] In this invention, when the active substance of the pharmaceutical composition is STK26 protein, it is administered via tail vein injection or intravenous infusion; when the active substance is the encoding gene of STK26 protein, it is administered by overexpressing or knocking out the encoding gene of STK26 protein in osteoclasts.

[0029] This invention also provides the application of the STK26 gene in regulating osteoclast function, wherein the regulation of osteoclast function is the regulation of changes in bone metabolism.

[0030] This invention also provides a method for regulating osteoclast differentiation, which involves knocking out the STK26 gene and using a modified lentivirus to carry the STK26 gene and target it to osteoclasts, thereby knocking out the STK26 gene in osteoclasts and reducing osteoclast differentiation.

[0031] Example 1: Upregulation of STK26 Expression in Peripheral Blood Mononuclear Cells of Clinical Osteoporosis Patients. To investigate the role of MST4 in the development of osteoporosis and its potential regulatory mechanisms, we collected data from 60 osteoporosis patients, including 30 patients with a history of fractures and 30 patients without a history of fractures, and compared them with 60 healthy controls. We measured lumbar spine bone mineral density (T-score) and analyzed peripheral blood samples. We used quantitative real-time polymerase chain reaction (qPCR) and Western blotting to analyze the peripheral blood samples to determine the expression levels of the STK26 (MST4) gene and protein.

[0032] The results showed that, compared with the control group, the STK26 (MST4) mRNA and protein levels in osteoporosis patients were significantly increased (e.g., ...). Figure 1 AC), while the osteoporosis group had a significantly lower bone mineral density T-score (AC). Figure 1 D). Bone metabolism markers in peripheral blood were detected by enzyme-linked immunosorbent assay (ELISA), including bone formation markers P1NP and OC, and bone resorption markers β-CTX and TRAcP 5b.

[0033] Studies have found that osteocalcin (OC) levels are significantly lower in patients with osteoporosis, while there is no significant difference in the level of type I procollagen N-terminal propeptide (P1NP). Figure 1 EF). Furthermore, the levels of β-CTX and TRAP5b in patients with osteoporosis were significantly higher than in the control group (EF). Figure 1 GH).

[0034] Further Pearson correlation analysis showed that MST4 mRNA expression levels in osteoporosis patients were negatively correlated with serum bone mineral density and bone metabolism markers (r = 0.71 and r = 0.65), but not significantly correlated with P1NP levels (r = 0.20). Figure 2 Furthermore, MST4 mRNA expression was positively correlated with bone resorption markers β-CTX (r=0.68) and TRAcP 5b (r=0.77) (Figure 2D-E).

[0035] Finally, a simple logistic regression analysis was performed on the relationship between MST4 mRNA expression level and fracture incidence in osteoporosis patients. The ROC curve results showed an AUC value of 0.8111 (Figure 1I), indicating that MST4 mRNA expression level has high reliability as a predictive indicator of fracture risk in osteoporosis patients. This also showed that MST4 expression in peripheral blood was significantly elevated. The number of monocytes in osteoporosis patients was negatively correlated with bone mineral density and bone formation, but positively correlated with bone resorption.

[0036] Example 2: Overexpression of STK26 (MST4) accelerates bone loss in ovariectomized mice, while knockout of the STK26 (MST4) gene alleviates bone loss in ovariectomized mice. Four-week-old C57BL / 6 mice were randomly divided into four groups of six each. After a two-day acclimatization period, sodium pentobarbital was administered intraperitoneally at a dose of 50 mg / kg. OVX was then performed to establish an osteoporosis model. Three days post-surgery, lentivirus was administered via tail vein for gene knockout and overexpression at a 10-fold fold increase, with a working titer of approximately 1 × 10⁻⁶. 9 TU / mL.

[0037] The ovariectomized mouse model was established by selecting 4-week-old and 24-week-old female C57BL / 6J mice.

[0038] 1) Incision and exposure of the ovary Incision location: Dorsal approach, make longitudinal incisions 1 cm to the sides of the spine, with an incision length of 0.5-1 cm, and bluntly dissect the muscle layer.

[0039] Locating the ovary: Gently grasp the fat pad above the uterine horn with forceps to pull out the cauliflower-shaped ovary.

[0040] 2) Ovarian removal Ligation of blood vessels: Use absorbable sutures to ligate the fallopian tube 0.5 cm proximal to the junction of the fallopian tube and the uterine horn.

[0041] Ovarian removal: The uterine horn distal to the ligation point is cut, and the ovary and its surrounding tissues are completely removed.

[0042] Contralateral procedure: Repeat the same steps to remove the other ovary.

[0043] 3) Suturing and Cleaning Layer-by-layer suturing: First suture the muscle layer (peritoneum), then suture the skin, and disinfect twice with iodine solution.

[0044] Sham surgery group: only the fat pad was pulled to simulate the operation, without ligation and excision.

[0045] Mice were divided into four groups: sh-NC + oe-NC (control); OVX + sh-NC + oe-NC (OVX); OVX + sh-MST4 + oe-NC (OVX + sh-MST4); and OVX + sh-NC + oe-MST4 (OVX + oe-MST4).

[0046] Wherein: sh-NC is the lentivirus knockout blank control group, oe-NC is the lentivirus overexpression blank control group, OVX is the ovariectomized mouse, sh-MST4 is the MST4 knockout lentivirus, and oe-MST4 is the MST4 overexpression lentivirus.

[0047] Bilateral ovariectomy was performed in mice in the OVX (mouse ovariectomy model), OVX (mouse ovariectomy model) + sh- MST4, and OVX + oe- MST4 groups, while the control group underwent only laparotomy without ovariectomy. Postoperatively, the corresponding lentivirus was injected via tail vein (Figure 3A).

[0048] At week 8, mice were euthanized and samples were collected to confirm the successful establishment of the ovariectomy (OVX) model, as mice undergoing OVX surgery exhibited complete bilateral ovarian absence and significant uterine atrophy (Figure 3B). To assess the in vivo efficacy of MST4 knockdown and overexpression, we measured blood counts (white blood cells, red blood cells, and platelets) (Figure 4A) and serum biochemical parameters (albumin, amylase, alkaline phosphatase, blood urea nitrogen, calcium, creatinine, globulin, glucose, potassium, sodium, phosphorus, total bilirubin, and total protein) (Figure 4B). Before sacrifice at week 8, the results for the OVX+sh-NC+oe-NC (OVX) group and the OVX+sh-MST4+oe-NC (OVX+sh-MST4) group were consistent across groups, confirming the effectiveness of MST4 gene knockdown and overexpression in vivo. Western blot analysis of the tibia revealed significantly elevated expression of MST4 and bone metabolism markers (including c-Fos, NFATc1, and TRAP proteins) in OVX mice. Silencing MST4 led to downregulation of these markers, while overexpression of MST4 had the opposite effect (Figure 3C).

[0049] Microcomputed tomography (CT) analysis of the femurs of these mice revealed that ovariectomy significantly reduced bone mineral density, trabecular bone number, trabecular bone thickness, and trabecular spacing. Silencing the MST4 protein reversed these trends, while overexpression of the MST4 protein exacerbated these changes (Figures 5A-B). Consistent with the CT results, hematoxylin and eosin (H&E) staining confirmed the protective effect of MST4 silencing against bone loss in ovariectomized mice (Figure 5C). To investigate whether MST4 silencing improved ovariectomy-induced bone loss by inhibiting bone resorption in vivo, TRAP staining was performed on femoral sections. The results showed a significant increase in the number of TRAP+ multinucleated osteoclasts (N.Oc / BS) and the ratio of osteoclast area to bone surface area in mice after ovariectomy, confirming the enhanced osteoclast formation and activity induced by ovariectomy.

[0050] However, these changes were suppressed by MST4 silencing, while MST4 overexpression promoted them. Figure 5 DE). Finally, a three-point bending test was performed to assess the maximum load and stiffness of the mouse femur. Consistently, ovariectomy reduced the maximum load and stiffness of the mouse femur. Femur stiffness significantly increased after MST4 silencing, but decreased again after MST4 overexpression (Fig. 5F).

[0051] Example 3: Silencing STK26 (MST4) can improve age-related bone loss and enhance bone strength in mice. An age-related osteoporosis model was established using 2-month-old and 24-month-old C57BL / 6 mice.

[0052] The method for establishing an age-related osteoporosis model is as follows: Two-month-old C57BL / 6 mice were selected as the young group, and 24-month-old C57BL / 6 mice were selected as the old group.

[0053] Rearing environment: SPF-grade barrier, temperature 22–25℃, humidity 50–60%, 12-hour light cycle (≤300 lux).

[0054] Feed: Standard maintenance diet (calcium content 0.6–1.0%), the elderly group needs to be supplemented with vitamin D (800 IU / kg) to prevent secondary bone loss.

[0055] C57BL / 6 mice were divided into four groups (Young, Old, Old+sh-MST4, and Old+oe-MST4). Lentiviral virus was administered via tail vein injection (Figure 6A), followed by euthanasia and sampling to confirm the successful establishment of an age-related osteoporosis model. Western blot analysis of the tibia showed significantly increased expression of MST4 and bone metabolism markers, including c-Fos, NFATc1, and TRAP proteins, in the Older group compared to the Younger group. Silencing MST4 led to downregulation of these markers, while overexpression of MST4 produced the opposite effect (Figure 6B).

[0056] Microcomputed tomography (CT) analysis of the femurs of these mice revealed significantly reduced bone mineral density, trabecular bone number, trabecular bone thickness, and trabecular spacing in the aged group. Silencing the MST4 protein reversed these trends, while overexpression of the MST4 protein exacerbated these changes (Figures 6C-D). Consistent with the CT results, hematoxylin and eosin (H&E) staining confirmed the protective effect of MST4 silencing against age-induced bone loss (Figure 6E). To investigate whether MST4 silencing improves age-induced bone loss by inhibiting bone resorption in vivo, TRAP staining was performed on femoral sections. The results showed a significant increase in the number of TRAP+ multinucleated osteoclasts (N.Oc / BS) and the ratio of osteoclast area to bone surface area in the aged group mice. However, these changes were suppressed by MST4 silencing, while MST4 overexpression promoted these changes (Figures 6F-G). Finally, a three-point bending test was performed to assess the maximum load and stiffness of the mouse femur. Consistently, compared with the young mice, the aged mice showed reduced maximum load and stiffness of the femur, which significantly increased after MST4 silencing but decreased again after MST4 overexpression (Fig. 6H).

[0057] These results are consistent with the osteoporosis phenotype observed in the OVX model. These results indicate that STK26 (MST4) plays a crucial role in age-related bone loss, and silencing STK26 can improve age-related bone loss and enhance bone strength.

[0058] The specific embodiments described above further illustrate the purpose, technical solution, and beneficial effects of the present invention. It should be understood that the above description is only a specific embodiment of the present invention and is not intended to limit the scope of protection of the present invention. Any modifications, equivalent substitutions, improvements, etc., made within the spirit and principles of the present invention should be included within the scope of protection of the present invention.

Claims

1. The application of the STK26 gene in the preparation of drugs for the treatment or prevention of osteoporosis, characterized by: Application of STK26 protein or its encoding gene in the preparation of drugs for the treatment or prevention of osteoporosis.

2. The application of the STK26 gene according to claim 1 in the preparation of drugs for treating or preventing osteoporosis, characterized in that: The amino acid sequence of the STK26 protein is shown in SEQ ID No. 1, and the coding gene sequence of the STK26 protein is shown in SEQ ID No.

2.

3. The application of the STK26 gene according to claim 1 in the preparation of drugs for treating or preventing osteoporosis, characterized in that: STK26 protein is used to prepare drugs for the treatment of osteoporosis, which are administered via intravenous infusion or tail vein injection.

4. The application of the STK26 gene according to claim 1 in the preparation of drugs for treating or preventing osteoporosis, characterized in that: When preparing drugs for treating osteoporosis by specifically knocking out the STK26 protein encoding gene in osteoclasts, the drug is administered.

5. The application of the STK26 gene according to claim 4 in the preparation of drugs for treating or preventing osteoporosis, characterized in that: When preparing drugs for treating osteoporosis, the STK26 protein encoding gene is introduced into osteoclasts via a lentiviral vector.

6. The application of the STK26 gene according to claim 1 in the preparation of drugs for treating or preventing osteoporosis, characterized in that: STK26 protein or its encoding gene can be used as a target for clinical drug therapy.

7. A pharmaceutical composition for treating or preventing osteoporosis, characterized in that: The active substance in the pharmaceutical composition is the STK26 protein and its encoding gene.

8. The pharmaceutical composition for treating or preventing osteoporosis according to claim 7, characterized in that: When the active substance of the drug composition is STK26 protein, it is administered via tail vein injection or intravenous infusion; when the active substance is the encoding gene of STK26 protein, it is administered by overexpressing or knocking out the encoding gene of STK26 protein in osteoclasts.

9. The application of the STK26 gene in regulating osteoclast function, characterized in that, The regulation of osteoclast function refers to the regulation of changes in bone metabolism.

10. A method for regulating osteoclast differentiation, characterized in that, By knocking out the STK26 gene and using a modified lentivirus to carry the STK26 gene and target it to osteoclasts, the STK26 gene in osteoclasts is knocked out, reducing osteoclast differentiation.

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