Application of C8orf76 as target to preparation of targeted medicine for preventing or treating colon cancer

Abstract

The invention relates to the technical field of biological medicine, and provides application of C8orf76 serving as a target spot in preparation of targeted drugs for preventing or treating colon cancer, screening of drugs capable of inhibiting C8orf76 serving as the target spot is included, the drugs are used for preventing or treating the colon cancer, a new strategy and a new direction are provided for treatment of the colon cancer, and a better treatment effect is brought to a patient with the colon cancer. By means of the technical scheme, the problem that in the prior art, a colon cancer treatment method is poor in treatment effect is solved.

Description

TECHNICAL FIELD

[0001] The present application relates to the technical field of biological medicine, in particular, relates to the application of C8orf76 as a target in the preparation of a targeted drug for preventing or treating colon cancer. BACKGROUND

[0002] Colon cancer is a malignant tumor that occurs in the colon. The colon is the main part of the large intestine, starting from the ileocecal junction, followed by ascending colon, transverse colon, descending colon and sigmoid colon. Colon cancer is a tumor formed by abnormal cell proliferation due to genetic mutation of colon mucosa epithelial cells. It is one of the common malignant tumors in the digestive system and one of the highest incidence and mortality rates of cancer worldwide. The occurrence of colon cancer is usually related to multiple factors, including genetic factors, dietary habits, lifestyle and certain chronic intestinal diseases.

[0003] Current treatment methods for colon cancer usually include surgery, radiotherapy, chemotherapy, etc. Different methods are selected for treatment according to the patient's condition. Despite the various treatment methods, the prognosis of colon cancer patients is still poor. Therefore, discovering new regulatory genes related to the occurrence of colon cancer is of great significance for further exploring the biological characteristics of colon cancer and the research of anti-colon cancer targeted drugs. SUMMARY

[0004] The present application proposes the application of C8orf76 as a target in the preparation of a targeted drug for preventing or treating colon cancer, solving the problem of poor treatment effect of the existing colon cancer treatment method.

[0005] The technical solution of the present application is as follows: The present application proposes the application of C8orf76 as a target in the preparation of a targeted drug for preventing or treating colon cancer.

[0006] As a further technical solution, the application includes screening a targeted drug for preventing or treating colon cancer with the C8orf76 as a target.

[0007] As a further technical solution, the screening is specifically screening a drug capable of inhibiting the expression amount of the C8orf76.

[0008] As a further technical solution, the targeted drug for preventing or treating colon cancer includes an inhibitor of C8orf76.

[0009] As a further technical solution, the structural formula of the inhibitor of C8orf76 is as follows: Compound acarbose: ; Compound troxerutin: ; Compound chlorogenic acid: Compound coenzyme A: Compound glycyrrhizic acid:

[0010] As a further technical solution, the prevention or treatment of colon cancer targeted drugs also include pharmaceutically acceptable excipients.

[0011] As a further technical solution, the excipients include one or more of diluents, wetting agents, binders, lubricants, colorants, coating agents.

[0012] As a further technical solution, the dosage form of the prevention or treatment of colon cancer targeted drugs includes one or more of tablets, capsules, granules, pills, injections, powders, suspensions.

[0013] The application also provides the use of C8orf76 as a target in the preparation of a kit for diagnosing colon cancer.

[0014] As a further technical solution, the kit can detect the expression amount of C8orf76.

[0015] The working principle and beneficial effects of the application are: 1. In the application, it is found for the first time that C8orf76 is highly expressed in colon cancer tissue, and knocking out C8orf76 can effectively reduce the proliferation and migration rate of colon cancer cells, inhibit the tumor formation ability of cells, indicating that C8orf76 plays an important role in the pathogenesis of colon cancer, and can be used as a new molecular marker and drug target for the diagnosis and treatment of colon cancer. Therefore, the drug for inhibiting the function of C8orf76 is prepared by taking C8orf76 as a target, the purpose of preventing or treating colon cancer is achieved, a new strategy and direction for the treatment of colon cancer are provided, better treatment effect is brought to colon cancer patients, and high clinical application value is obtained.

[0016] 2. In the application, it is found that C8orf76 can be used as a target of small molecule drugs for preventing and treating colon cancer, and based on this, five small molecule drugs (acarbose, troxerutin, chlorogenic acid, coenzyme A, glycyrrhizic acid) acting on the C8orf76 target are provided through virtual screening and biological verification. Experiments show that these small molecule drugs as C8orf76 inhibitors have high anti-colon cancer effect. BRIEF DESCRIPTION OF DRAWINGS

[0017] The application will be further described in detail below in combination with the drawings and specific embodiments.

[0018] Figure 1 ​​​This is a comparison image of immunofluorescence staining of C8orf76 in human colon cancer tissue samples and adjacent non-cancerous tissues in Example 1 of the present invention; Figure 2 The figure shows the experimental results of the effect of the C8orf76 inhibitor on cell proliferation in Example 4 of this invention; In the left figure, NC represents the SW1116 wild-type colon cancer cell group, NC+ACA represents the SW1116 wild-type colon cancer cell group + acarbose treatment group, C8orf76 represents the C8orf76 overexpressing SW1116 colon cancer cell group, and C8orf76+ACA represents the C8orf76 overexpressing SW1116 colon cancer cell group + acarbose treatment group. In the right figure, NC represents the SW1116 wild-type colon cancer cell group, NC+ACA represents the SW1116 wild-type colon cancer cell group treated with coenzyme A, C8orf76 represents the C8orf76 overexpressing SW1116 colon cancer cell group, and C8orf76+ACA represents the C8orf76 overexpressing SW1116 colon cancer cell group treated with coenzyme A. Figure 3 This is an electrophoresis diagram of genotype PCR identification in Example 4 of the present invention; In the figure, WT is a C56BL6 / J wild-type mouse, HO is a C57BL / 6J-C8orf76 humanized knock-in mouse, H20 is a negative water control, and the marker is a 100bp Plus DNA Ladder from Transgen (model BM311-01). Figure 4 This is a diagram illustrating the therapeutic effect of the C8orf76 inhibitor in a colorectal cancer animal model in Example 5 of the present invention. In the figure, WT is C56BL6 / J wild-type mouse, HO is C57BL / 6J-C8orf76 humanized knock-in mouse, Ctrl is the untreated group, ACA is the acarbose-treated group, AOM / DSS is the colorectal cancer model group, and AOM / DSS+ACA is the colorectal cancer model + acarbose-treated group. Figure 5 This is a tumor data graph illustrating the therapeutic effect of the C8orf76 inhibitor in a colorectal cancer animal model in Example 5 of the present invention. In the figure, WT represents C56BL6 / J wild-type mice, HO represents C57BL / 6J-C8orf76 humanized knock-in mice, Ctrl represents the untreated group, ACA represents the acarbose-treated group, AOM / DSS represents the colorectal cancer model group, and AOM / DSS+ACA represents the colorectal cancer model + acarbose-treated group. Detailed Implementation

[0019] The technical solutions of the present invention will be clearly and completely described below with reference to the embodiments of the present invention. Obviously, the described embodiments are only some embodiments of the present invention, and not all embodiments. Based on the embodiments of the present invention, all other embodiments obtained by those of ordinary skill in the art without creative effort are within the scope of protection of the present invention.

[0020] Example 1: Expression and distribution of C8orf76 protein in human colon cancer tissue samples 1.1 Experimental Methods Postoperative colon cancer tissue samples from colorectal cancer patients were fixed overnight in paraformaldehyde, dehydrated with 30wt% sucrose, and then frozen on a -20℃ freezing stage using OCT embedding medium. The frozen tissue blocks were trimmed, and the pre-cut thickness was adjusted according to different tissue types. The sections were air-dried at room temperature before subsequent staining. The tissues were dewaxed and rehydrated in the following order: xylene I (10 min), xylene II (10 min), xylene III (10 min), anhydrous ethanol I (5 min), anhydrous ethanol II (5 min), 95% ethanol (3 min), 90% ethanol (3 min), 80% ethanol (2 min), 70% ethanol (2 min), distilled water I (3 min), and distilled water II (3 min). Citrate antigen retrieval solution (pH 6.0) was prepared and processed using a microwave oven. For antigen retrieval, first heat at medium-high (80% power) for 8 minutes, then heat off for 8 minutes, and finally heat at medium-low (50% power) for 7 minutes. After natural cooling, wash three times with PBS buffer, 5 minutes each time. After washing, gently blot dry, and use a histochemical pen to draw a circle around the tissue, enclosing the entire tissue. Then, add goat serum and block at room temperature for 1 hour. After blocking, wash three times with PBS buffer, 5 minutes each time. Add rabbit anti-human C8orf76 fluorescent primary antibody (model bs-15301R) to cover the entire tissue, and incubate overnight at 4°C. After incubation, wash three times with PBS buffer (pH 7.3), 5 minutes each time. Add goat anti-rabbit fluorescent secondary antibody to cover the entire tissue, and incubate in a dark box at room temperature for 1 hour. After incubation, wash three times with PBS buffer (pH 7.3), 5 minutes each time. 7.3) Wash three times, 5 min each time; stain with DAPI (4',6-diamidinyl-2-phenylindole) solution at room temperature in the dark for 10 min, then wash three times with PBS buffer, 5 min each time. Gently pat dry, add anti-fluorescence attenuation mounting medium, cover with a coverslip, and observe the distribution of the target protein C8orf76 under a microscope.

[0021] 1.2 Experimental Results Observation results as follows Figure 1As shown in the figure, the protein expression level of C8orf76 is higher in tumor tissue compared with adjacent normal tissue; according to ImageJ software analysis, the positive expression rate of C8orf76 in human colon cancer tissue is as high as 73.4%.

[0022] Example 2: Effects of C8orf76 on the function of colon cancer cells 2.1 Cell proliferation experiment SW620 cells were divided into a C8orf76 overexpression group (experimental group) and an overexpression control group (control group); SW1463 cells were divided into a blank group, a C8orf76 knockout group (experimental group), and a knockout control group (control group). The C8orf76 overexpression group (experimental group) and the overexpression control group (control group) were obtained according to the method of Guo S, Liu CC, Zhao ZF, Li ZX, Jiang X, Zhao ZR. Chromosome 8 Open Reading Frame 76 (C8orf76) Co-Expressed with Cyclin-Dependent Kinase 4 (CDK4) as a Prognostic Indicator of Colorectal Cancer. Biomed Environ Sci. 2025;38(8):977-987. The overexpression group was transfected with pcDNA3.1-C8orf76, and the overexpression control group was transfected with the empty vector pcDNA3.1.

[0023] The C8orf76 knockout group (experimental group) and knockout control group (control group) were obtained according to the method of Wang XH, LiangQY, Zhang LH, Gou HY, Li ZY, Chen HR, Dong YJ, Ji JF, Yu J. C8orf76 Promotes Gastric Tumorigenicity and Metastasis by Directly Inducing lncRNA DUSP5P1 and Associates with Patient Outcomes. Clin Cancer Res. 2019 May 15;25(10):3128-3140. The C8orf76 knockout group was transfected with the shC8orf76 vector, and the knockout control group was transfected with the negative control shNC vector.

[0024] The colon cancer cells were seeded into 96-well plates with 100 μL of cell suspension per well (approximately 1000 cells per well; no cells were added to the control wells). After incubating the cells at 37°C in a cell culture incubator with 5% CO2 air and 100% humidity for 72 hours, 10 μL of CCK-8 solution was added to each well. After adding the CCK-8 solution, the 96-well plates were returned to a 37°C, 5% CO2 incubator for 3 hours. The absorbance (OD value) of each well was measured at 450 nm using a microplate reader. The relative cell viability (%) was calculated using the following formula: (OD experiment - OD blank) / (OD control - OD blank) × 100%, where OD experiment is the absorbance value of the experimental group, OD blank is the absorbance value of the blank group, and OD control is the absorbance value of the control group.

[0025] 2.2 Cell migration experiment Cells were cultured to a density of 90%–95%; a straight "scratch" of approximately 0.5 mm was made in the cell layer using a 200 μL pipette tip; the cell layer was washed with PBS buffer (pH 7.3) and then incubated with culture medium for 24 h; images of the scratch at fixed locations were taken under a microscope, and the changes in scratch width were analyzed using ImageJ. The final results were expressed as relative cell migration values. Relative cell migration value = (overexpression group - control group) / control group.

[0026] 2.3 Subcutaneous tumor formation experiment in BALB / c mice Five-week-old BALB / c mice (n=6 / group) were purchased and fed normally for one week. On day 1 of the experiment, 1×10⁶ murine colon cancer cells were injected under the armpit. 6 One; measure the tumor size daily, until the tumor size reaches 100mm. 3 Observe and record the body weight and tumor growth of the mice after treatment; terminate the experiment on day 15, take tumor tissue, observe and measure the volume of intestinal tumors in the experimental group and control group mice and take pictures.

[0027] 2.4 Experimental Results The experimental results regarding the effect of C8orf76 on colon cancer cell function are shown in Table 1 below: Table 1. Effects of C8orf76 on colon cancer

[0028] As shown in Table 1, C8orf76 overexpression promotes the proliferation and migration of colon cancer cells and tumorigenesis in mice, while knockout of C8orf76 inhibits the proliferation and migration of human colon cancer cells and tumorigenesis in mice.

[0029] Example 3: Screening of C8orf76-targeting inhibitors Inhibitors targeting the C8orf76 protein were virtually screened. The software used for virtual screening was Schrödinger Maestro 11.4, and the 3D plotting software was PyMol. The screening process is as follows: Protein preparation: The predicted 3D structure of C8orf76 (AlphaFold ID: AF-Q96K31-F1) was downloaded from the AlphaFold database. The protein preparation wizard module was used to optimize the structure, followed by energy optimization (OPLS2005 force field, RMSD of 0.3 Å). Binding sites were predicted using the Sitemap module. A grid file was created using the Receptor GridGeneration module, centered on Site1 (key amino acid residues HIS105 / GLY209 / ARG66 / SER142 / THR293), with all bin sizes set to 20 Å × 20 Å × 20 Å.

[0030] Compound preparation: The 2D formats of the MCE Bioactive Compound Library (containing 18.7K compounds), MCE 50K Diversity Library (containing 50.0K compounds), and Natural Product Library (containing 3904 compounds) were processed by hydrogenation, energy optimization, etc. in the LigPrep Module of Schrödinger software to output 3D structures for virtual screening.

[0031] Molecular docking: The Virtual Screening Workflow module was used for virtual screening. Prepared compounds were imported, and molecular docking was performed using the Glide module, where acceptor and ligand molecules dock with each other through geometric and energy matching. First, the high-throughput screening (HTVS) mode in the Glide module was used to screen small molecule compounds from the MCE 50K DiversityLibrary. The top 10% of small molecule compounds were selected for a second round of screening using the standard (SP) mode. Then, the top 10% were selected for a third round of screening using the high-precision (XP) mode, resulting in a ranking of the small molecule compounds. 18.7 K compounds from the MCE Bioactive Compound Library were docked with the target protein C8orf76 Human CKMT in HTVS mode. The top 15% of small molecule compounds by score were selected for a second round of screening using standard (SP) mode. Subsequently, the top 15% were selected for a third round of screening using high-precision (XP) mode to obtain the ranking of small molecule compounds. The standard (SP) mode of the compound Glide module in the Natural Product Library was used for the first round of screening. Subsequently, the top 15% of molecules by score were selected for a second round of screening using high-precision (XP) mode. All screening results were output to obtain the ranking of small molecule compounds. Finally, the binding force between the target and the compound, the compound structure, etc., were manually verified, and the top 200 compounds in the MCE 50K Diversity Library, the MCE Bioactive Compound Library, and the Natural Product Library were selected and output. Furthermore, the compounds were selected to be plotted with the C8orf76 protein.

[0032] The affinity of the screened small molecules for C8orf76 was determined using surface plasmon resonance, as detailed below: Each analyte was diluted to several concentrations in a 96-well plate and coupled to the target protein C8orf76 via a chip from low to high concentration at a flow rate of 30 μL / min for 150 s.

[0033] After each concentration point is run, the chip is regenerated for 5 minutes with 10 mM glycine salt (pH 2.0) solution. This process is repeated until all the corresponding concentrations of the analytes have been run.

[0034] By using Biacore Insight evaluation software (Cytiva, Marlborough, MA, USA), the data were globally fitted to a 1:1 Langmuir binding model to obtain the binding and dissociation constants.

[0035] The five small molecule compounds with the strongest affinity (i.e., five small molecule inhibitors) were selected, and their structural formulas are as follows: Compound acarbose: ; The compound troxerutin: ; The compound chlorogenic acid: ; Compound Coenzyme A: ; The compound glycyrrhizic acid: ; The binding affinity and docking fraction of the above five small molecule inhibitors with C8orf76 are shown in the table below: Table 2. Binding affinity and docking fraction of the five screened small molecule inhibitors with C8orf76

[0036] Note: KD: dissociation constant, which reflects the affinity of the analyte for the target; the smaller the value, the stronger the affinity. Ka: binding rate constant, which represents the speed of intermolecular binding; the larger the value, the faster the binding. Kd: dissociation rate constant, which represents the speed of intermolecular dissociation; the larger the value, the faster the dissociation.

[0037] Example 4: Inhibitory effect of small molecule inhibitors targeting and binding to C8orf76 on the function of C8orf76-overexpressing colon cancer cells. The following experiment was conducted using two small molecule inhibitors, acarbose and coenzyme A, as examples: 4.1 Cell proliferation experiment The method for obtaining C8orf76-overexpressing SW1116 colorectal cancer cells was performed according to the method described by Guo S, Liu CC, Zhao ZF, LiZX, Jiang X, Zhao ZR. Chromosome 8 Open Reading Frame 76 (C8orf76) Co-Expressed with Cyclin-Dependent Kinase 4 (CDK4) as a Prognostic Indicator of Colorectal Cancer. Biomed Environ Sci. 2025;38(8):977-987.

[0038] 100 μL of SW1116 wild-type colon cancer cells or C8orf76-overexpressing SW1116 colon cancer cells (i.e., 1000 cells per well) were added to each well of a 96-well plate. The experimental group received either the inhibitor acarbose or coenzyme A, while the control group received no inhibitor. The inhibitor dosages were acarbose (5 μM) and coenzyme A (200 μM). The 96-well plates were incubated at 37°C in a cell culture incubator with 5% CO2 air and 100% humidity for 0 h, 24 h, 48 h, and 72 h. 10 μL of CCK-8 solution was added to each well. After adding the CCK-8 solution, the 96-well plates were returned to the 37°C, 5% CO2 incubator for 3 h. The absorbance (OD value) of each well was measured at 450 nm using a microplate reader. The results are shown below. Figure 2 The relative cell survival rate (%) was calculated according to the following formula: (OD inhibitor - OD blank) / (OD control - OD blank) × 100%. The results are shown in Table 3. In the formula, the OD inhibitor is the absorbance value of the experimental group, the OD blank is the absorbance value of the blank group, and the OD control group is the absorbance value of the control group.

[0039] Table 3. Inhibitory effect of small molecule inhibitors on the proliferation of C8orf76-overexpressing colon cancer cells.

[0040] Depend on Figure 2 As shown in Table 3, acarbose and coenzyme A had no significant effect on the proliferation of wild-type colorectal cancer cells, while treatment with acarbose and coenzyme A could inhibit the proliferation of C8orf76-overexpressing colorectal cancer cells.

[0041] 4.2 AOM / DSS-induced colon cancer experiment in C57BL / 6 mice Animals: C57BL / 6J wild-type mice (WT) and C57BL / 6J-C8orf76 humanized knock-in mice (HO).

[0042] The C57BL / 6J-C8orf76 humanized knock-in mouse was created through gene editing using CRISPR / Cas9 technology in collaboration with Nanmo Biotechnology Co., Ltd., with the element CAG-LSL-C8orf76-WPRE-polyA inserted at the Rosa26 site. This element was then used in combination with tissue-specific Cre mice to construct the C57BL / 6J-C8orf76 humanized knock-in mouse. After construction, the genotype of the C57BL / 6J-C8orf76 humanized knock-in mouse was identified using the following methods: Extracting genomic DNA from C57BL / 6J-C8orf76 humanized knock-in mice: Cut off mouse tails (approximately 0.5 cm in length) and place them in pre-labeled 1.5 mL centrifuge tubes, capping them tightly. Add 0.5 mL of lysis buffer and 50 µL of proteinase K stock solution to each tube and tighten the cap. Place the centrifuge tubes in a hybridization oven at 56°C overnight. The next day, centrifuge the samples at 12000 rpm for 10 minutes at room temperature. Pour the supernatant into 1.5 mL Eppendorf tubes, add 1 mL of anhydrous ethanol (approximately twice the volume of the supernatant), tighten the cap, and gently shake; a flocculent precipitate will be visible. Centrifuge at 13000 rpm for 15 minutes and discard the supernatant. Add 1 mL of 70% ethanol, wash, centrifuge at 13000 rpm for 10–15 minutes, discard the supernatant, collect the precipitate, and allow it to air dry at room temperature for 15 minutes. Add 80–100 µL of sterile water to each tube, cap, and incubate at room temperature or 37°C for 1 hour to fully dissolve. After the DNA has completely dissolved, leave the container at room temperature for several hours and then store it at -20°C, or proceed directly to PCR or hybridization experiments. If the DNA is not completely dissolved, it can be placed in a 37°C water bath for 30-60 minutes, but not overnight. The DNA concentration should be controlled between 50-100 ng / µL, and the OD260 / 280 ratio should be between 1.8 and 2.0.

[0043] PCR identification: PCR identification was performed using extracted mouse genomic DNA as a template. The primers, PCR reaction system, and PCR reaction conditions used for PCR identification are shown in Table 4 below. Table 4 Primer sequences, PCR reaction system, and PCR reaction conditions used for PCR amplification

[0044] PCR identification electrophoresis image as shown Figure 3 As shown.

[0045] Colorectal cancer model group (AOM / DSS): Five-week-old mice (n=6 / group) were fed normally for one week; then, they were intraperitoneally injected with AOM (azomethane, 10 mg / kg); in the second week of the experiment, a 1.5 wt% DSS (sodium dextran sulfate) solution was prepared and allowed to be drunk freely for one week, and diarrhea and bloody stools were observed and recorded after drinking DSS; for the next two weeks, they were restored to a normal diet. The above steps (from intraperitoneal injection of AOM to restoration of a normal diet) were repeated for 3 cycles, 3 times, to simulate the process of carcinogenesis in human ulcerative colitis. The experiment was terminated after 16 weeks.

[0046] Colorectal cancer model + acarbose treatment group (AOM / DSS+ACA): The colorectal cancer model was established in the same way as the colorectal cancer model group. Mice were given acarbose in drinking water every 4 days (acarbose concentration 0.125 mg / mL, acarbose dose / mice body weight ratio: 1 mg / 25 g), and the intervention was carried out periodically for 16 weeks to terminate the experiment. The mouse colon was isolated and the number of tumors was counted.

[0047] Table 5. Therapeutic effects of small molecule inhibitors in C8orf76-overexpressing colorectal cancer animal models

[0048] Depend on Figure 4 , Figure 5 As shown in Table 5, in AOM / DSS-induced colorectal cancer model mice, the tumor burden of C8orf76 overexpressing mice was significantly higher than that of wild-type mice. After treatment with acarbose, the C8orf76-mediated tumor-promoting effect was significantly inhibited, as evidenced by a reduction in the number of tumors.

[0049] The above are merely preferred embodiments of the present invention and are not intended to limit the present invention. Any modifications, equivalent substitutions, improvements, etc., made within the spirit and principles of the present invention should be included within the protection scope of the present invention.

Claims

1. Application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colorectal cancer.

2. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colorectal cancer according to claim 1, characterized in that, The application includes screening targeted drugs for the prevention or treatment of colon cancer using C8orf76 as a target.

3. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colon cancer according to claim 1, characterized in that, The screening specifically involves screening for drugs that can inhibit the function of C8orf76.

4. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colon cancer according to claim 3, characterized in that, The targeted drugs for the prevention or treatment of colon cancer include inhibitors of C8orf76.

5. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colon cancer according to claim 3, characterized in that, The structural formula of the C8orf76 inhibitor is as follows: or or or or .

6. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colon cancer according to claim 4, characterized in that, The targeted drugs for the prevention or treatment of colon cancer also include pharmaceutically acceptable excipients.

7. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colorectal cancer according to claim 6, characterized in that, The excipients include one or more of the following: diluent, wetting agent, adhesive, lubricant, colorant, and coating agent.

8. The application of C8orf76 as a target in the preparation of targeted drugs for the prevention or treatment of colon cancer according to claim 4, characterized in that, The dosage forms of the targeted drugs for the prevention or treatment of colorectal cancer include one or more of the following: tablets, capsules, granules, pills, injections, powders, and suspensions.

9. Application of C8orf76 as a target in the preparation of diagnostic kits for colorectal cancer.

10. The application of C8orf76 as a target in the preparation of a diagnostic reagent kit for colon cancer according to claim 9, characterized in that, The kit can detect the expression level of C8orf76.

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