22 results about "G1 phase" patented technology

A series of 1, 3, 5-triazine compounds that exhibit potent inhibition of endosomal trafficking and autophagy is provided. These compounds effectively suppress cancer cell proliferation, growth, and migration, induce cell cycle arrest at the G0 / G1 phase, promote cancer cell death via non-apoptotic pathways, and inhibit tumor sphere formation. Moreover, select compounds within this series demonstrate significant inhibition of tumor growth and metastasis in mouse models of lung cancer and melanoma. Additionally, they modulate macrophage polarization and the tumor microenvironment by regulating cytokine secretion. These findings highlight the potential of 1, 3, 5-triazine compounds as promising antitumor agents.

The invention provides application of a bisindole compound XQ-016 in treatment of osteosarcoma, and belongs to the technical field of biological medicines. The bisindole compound XQ-016 can inhibit proliferation, migration and invasion of tumor cells by adjusting an STAT3 / p53 signal channel, inducing G1 phase cell cycle arrest and inhibiting MMP2 / MMP9 expression, shows remarkable anti-tumor activity, is a promising treatment choice in tumor treatment, and can be used as an effective component in anti-tumor drugs.

The present disclosure concerns methods for treating pancreatic cancer cells with a combination of gemcitabine (GEM) and SapC-DOPS. In some aspects, GEM treatment preferentially targets G1 phase cells which are low in surface phosphatidylserine (PS), resulting in an increased median surface PS level of PDAC cells. Inversely, SapC-DOPS targets high surface PS cells which are predominantly in the G2 / M phase. In other aspects, a combination therapy on tumors in vivo with SapC-DOPS and GEM or Abraxane® (Abr) / GEM is demonstrated to significantly inhibit tumor growth and increases survival.

The present invention relates to a composition for protecting cells from endoplasmic reticulum (ER) stress and oxidative stress induced by ultrafine dust, comprising galangin as an active ingredient. Galangin, which is an active ingredient of the composition for cell protection of the present invention, alleviated an increase in reactive oxygen species, intracellular calcium, and ER stress-related proteins induced by ultrafine dust PM2.5. In addition, galangin counteracted PM2.5-induced cell cycle arrest at the G0 / G1 phase and restored cell cycle regulators and matrix metalloproteinases. As a result, galangin can enhance cell protection against PM2.5-induced ER stress and cell cycle arrest via reactive oxygen species. Therefore, it is suggested that the composition comprising galangin as an active ingredient of the present invention has great potential as a candidate for a preventive agent or a therapeutic agent for diseases related to ER stress and oxidative stress induced by PM2.5.

The application discloses application of a petroleum ether extract of a root of a roadside green plant in preparation of a drug for treating colorectal cancer by regulating a PI3K / AKT / MDM2 / p53 pathway. In the application, the petroleum ether extract of the root of the roadside green plant for treating colorectal cancer is obtained by petroleum ether reflux extraction of the root of the roadside green plant. Pharmacological experiments show that the petroleum ether extract of the root of the roadside green plant treats colorectal cancer by regulating the PI3K / AKT / MDM2 / p53 signal pathway through down-regulating p-PI3K / PI3K and p-AKT / AKT ratio, up-regulating p-MDM2 and down-regulating p53 level; the extract has an anti-malignant proliferation effect, induces G1 phase arrest by targeting CDK2, up-regulating p21, down-regulating Cyclin E1-CDK2 and Cyclin D1-CDK4; the extract induces HCT-116 cell apoptosis through a mitochondrial pathway by up-regulating Bax / Bcl-2, reducing ΔΨm, releasing Cyt C, activating Caspase-9 / 3 and cleaving PARP; the extract inhibits migration and invasion of HCT-116 cells by targeting MMP9, down-regulating MMP-2, MMP-9 and N-cadherin expression and up-regulating E-cadherin expression. In addition, the extract inhibits growth of a transplanted tumor in a nude mouse transplanted tumor model by inducing apoptosis of transplanted tumor cells.

This invention relates to the field of biomedical technology and discloses a biomarker for diagnosing polycystic ovary syndrome (PCOS) and its application. The diagnostic biomarker is circSPECC1(4), which is formed by reverse splicing and circularization of the fourth exon of the SPECCC1 gene. It has a length of 1580 nt and possesses a closed circular RNA structure. circSPECC1(4) is specifically highly expressed in ovarian granulosa cells of PCOS patients, and there is no significant difference in the mRNA expression level of its parent gene SPECCC1. circSPECC1(4) possesses RNase R nuclease resistance stability and is mainly located in the cytoplasm. Knocking down the expression of circSPECC1(4) can significantly promote apoptosis of ovarian granulosa cells and arrest the ovarian granulosa cell cycle at the G0 / G1 phase. This invention clearly demonstrates that circSPECC1(4) can serve as a specific diagnostic biomarker for PCOS, fully verifying the structural characteristics, expression specificity, and pathological regulatory function of this circular RNA, filling the gap in the existing field of PCOS diagnosis which lacks highly specific and stable molecular diagnostic targets.

The application discloses application of SGI-7079 in treating FLT3 mutant acute myeloid leukemia. The application research shows that SGI-7079 can be stably combined with FLT3, inhibit the phosphorylation level of FLT3 and downstream STAT5, AKT and ERK, and induce G1 phase arrest and cell apoptosis. In vitro, SGI-7079 has strong inhibitory effect on FLT3-ITD and drug-resistant mutant cells; in a FLT3-ITD mouse model, SGI-7079 can significantly reduce leukemia load and prolong survival, and shows better curative effect than existing drugs on drug-resistant mutations such as F691L and D835Y. Meanwhile, SGI-7079 also has significant inhibitory effect on primary cells of FLT3-ITD positive patients. It is shown that SGI-7079 can be used as a new drug candidate for treating FLT3 mutation and drug-resistant AML, and provides a new direction for optimizing targeted therapy strategy.

The application discloses an application of an indole dione piperazine compound in preparation of a drug for resisting prostate cancer. Experiments such as MTT, flow cytometry, protein chip, molecular docking, CETSA, transmission electron microscopy and zebra fish model prove that the compound significantly inhibits proliferation of prostate tumor cells such as PC-3, 22Rv1 and DU145, blocks division of PC-3 cells in the G1 phase, and induces apoptosis and necrotic apoptosis of PC-3 cells; the mechanism is that the compound directly combines NQO1 and NRF2, activates the HO-1 / NRF2 / NQO1 pathway, promotes excessive generation of ROS, and causes NQO1-dependent oxidative stress. The zebra fish model in vivo shows that the compound inhibits growth of prostate tumors. The application provides a lead compound with a new mechanism for preventing and treating prostate cancer and potential for overcoming drug resistance.

The invention belongs to the technical field of biological medicines, and particularly relates to application of genistein to preparation of an anti-colorectal cancer medicine for inhibiting LINC00355 expression. According to the present invention, the genistein is adopted as the LINC00355 expression inhibitor so as to effectively inhibit the expression of the LINC00355, such that the adsorption effect of the LINC00355 on the miR-150 is relieved, the expression of the miR-150 is up-regulated, the expression of the SGK1 is further inhibited by the miR-150, the activation of the downstream EGFR / PI3K / Akt and MAPK signal channels is finally inhibited, and the activity of the downstream EGFR / PI3K / Akt and MAPK signal channels is inhibited; and inhibition of colorectal cancer cell proliferation, inhibition of colorectal cancer cell cycle G0 / G1 phase, induction of colorectal cancer cell apoptosis and inhibition of colorectal cancer cell migration and invasion ability are realized, so that a better anti-colorectal cancer treatment effect is achieved.

The invention relates to application of JND7064 as AXL molecular glue to preparation of drugs for preventing or treating tumors related to AXL high expression, in particular to application of JND7064 to treatment of triple negative breast cancer. The JND7064 induces degradation of AXL through a CRBN dependent ubiquitin-proteasome pathway, and the JND7064 is combined with an AXL non-kinase structural domain. In addition, the JND7064 selectively inhibits the proliferation of the MDA-MB-231 cells, and the JND7064 induces the MDA-MB-231 to generate G0 / G1 phase retardation and induces the cells to generate apoptosis.

A series of 1,3,5-triazine compounds that exhibit potent inhibition of endosomal trafficking and autophagy is provided. These compounds effectively suppress cancer cell proliferation, growth, and migration, induce cell cycle arrest at the G0 / G1 phase, promote cancer cell death via non-apoptotic pathways, and inhibit tumor sphere formation. Moreover, select compounds within this series demonstrate significant inhibition of tumor growth and metastasis in mouse models of lung cancer and melanoma. Additionally, they modulate macrophage polarization and the tumor microenvironment by regulating cytokine secretion. These findings highlight the potential of 1,3,5-triazine compounds as promising antitumor agents.

The application discloses application of apolipoprotein III in prevention and treatment of Bombyx mori nuclear polyhedrosis virus infection and belongs to the cross field of molecular biology technology field and virus prevention and treatment. The application first finds that Bombyx mori apolipoprotein III (ApoLp-III) promotes biosynthesis and accumulation of ceramide, thereby inhibits mTORC1 signal pathway activity, induces cell G1 phase arrest, and effectively blocks a new mechanism of Bombyx mori nuclear polyhedrosis virus (BmNPV) replication. Based on the mechanism, the application provides application of ApoLp-III in inhibition of BmNPV proliferation, prevention and treatment of BmNPV infection, improvement of the ability of Bombyx mori to resist BmNPV or cultivation of a BmNPV-resistant Bombyx mori strain. The application provides a brand-new technical strategy and germplasm resource for realizing green, efficient and sustainable prevention and control of BmNPV.

The invention discloses an application of a diarrhea stopping capsule in preparation of a medicine for treating leukemia, the diarrhea stopping capsule can inhibit proliferation of leukemia cells HEL, KG-1a, K562 and Jurkat, and the inhibition effect on the cells HEL is dose-dependent and time-dependent; the drug-containing serum of the Xiaoshui capsule blocks the cell cycle of human erythroleukemia cells HEL in the G1 phase, and can obviously induce apoptosis of the human erythroleukemia cells HEL. Furthermore, in-vivo experiments show that low, medium and high dosages of the Xiaoshui capsules have no influence on liver and kidney functions of mice; the diarrhea stopping capsule can reduce the weight of the spleen of a mouse with leukemia, increase the hemolysis-to-solution ratio, improve the spleen structure, reduce the expression of a CD71 + cell population, promote differentiation of the spleen and immature red blood cells of bone marrow to a Ter119 + cell population and recover the spleen structure of the mouse. The Xiaoshui capsule is a clinical Miao medicine, can effectively shorten the preclinical research, and has a good application prospect in preparation of medicines for treating myelogenous and lymphatic leukemia.

The present application relates to the technical field of medicine, and particularly relates to application of ganoderma triterpene in preparation of medicine for treating cervical cancer. Ganoderma triterpene (Ganodecalone A, referred to as GDA) can inhibit migration, proliferation and clonogenic capacity of cervical cancer cells; GDA can arrest the cell cycle of cervical cancer cells in G0 / G1 phase, and with the increase of the concentration of GDA, the proportion of cells in G0 / G1 phase is significantly increased; GDA can promote apoptosis of cervical cancer cells, and with the increase of the concentration of GDA, the proportion of late apoptotic cells is significantly increased; GDA can promote apoptosis of cervical cancer cells by reducing the phosphorylation level of Akt in the cervical cancer cells. GDA and Akt phosphorylation agonist SC79 are mutually antagonistic, and when GDA is combined with Akt phosphorylation inhibitor MK-2206, the apoptosis of two strains of cervical cancer cells is promoted. GDA can induce apoptosis of cells by inhibiting phosphorylation of Akt, up-regulating pro-apoptotic protein Bad and down-regulating anti-apoptotic protein Bcl-2, and thus the anti-tumor effect is exerted.

The invention discloses an application of ursodesoxycholic acid UDCA in inhibition of Skp2 protein and resistance to non-small cell lung cancer, and particularly discloses an application of ursodesoxycholic acid UDCA in preparation of an Skp2 protein inhibitor, the ursodesoxycholic acid UDCA inhibits Skp2 to enable a cell cycle to be stagnated in a G0 / G1 phase, so that degradation of p21Cip1 and p27Kip1 is reduced. Meanwhile, the invention discloses application of ursodesoxycholic acid UDCA in preparation of a non-small cell lung cancer cell proliferation activity inhibitor. The ursodesoxycholic acid UDCA is reported to have relatively strong Skp2 protein inhibition capability and non-small cell lung cancer inhibition capability for the first time, is simple in structure, is one of main components of bile acid in bear gall powder, is also a chemical drug capable of being artificially synthesized, can be stably separated and extracted, and has a good application prospect. The compound is a natural antitumor compound which is efficient and easy to obtain.

The application discloses application of SGI-7079 in treating FLT3 mutant acute myeloid leukemia. The application research shows that SGI-7079 can be stably combined with FLT3, inhibit the phosphorylation level of FLT3 and downstream STAT5, AKT and ERK, and induce G1 phase arrest and cell apoptosis. In vitro, SGI-7079 has strong inhibitory effect on FLT3-ITD and drug-resistant mutant cells; in a FLT3-ITD mouse model, SGI-7079 can significantly reduce leukemia load and prolong survival, and shows better curative effect than existing drugs on drug-resistant mutations such as F691L and D835Y. Meanwhile, SGI-7079 also has significant inhibitory effect on primary cells of FLT3-ITD positive patients. It is shown that SGI-7079 can be used as a new drug candidate for treating FLT3 mutation and drug-resistant AML, and provides a new direction for optimizing targeted therapy strategy.

A significantly non-toxic novel mononuclear cobalt(III)-Schiff base complex (1) capable to induce apoptosis via G2-M cell cycle arrest in human breast cancer cell line MCF-7 and cell cycle arrest of colon cancer cell lines HCT-116 and SW-480 via G0-G1. The Schiff base complex (1) having >99% purity has been synthesized by a facile “One pot” synthesis method and has been characterized with standard spectroscopic techniques. Complex 1 exhibits cytotoxicity (IC50=16.81±1.33 μM) at much lower concentration in comparison to oxaliplatin (IC50=31.4±0.69 μM) against MCF-7 cells and causes apoptosis in colon cancer cell lines HCT-116 and SW-480 by arresting the cell cycle at the G0-G1 phase having IC50 values of 15.27±1.18 μM and 10.04±1.98 μM respectively comparable with the IC50 values of oxaliplatin which are 16.73±1.78 μM and 7.87±1.54 μM respectively after 24 h of treatment without being overly toxic to human PBMCs (IC50=>60 μM). In vivo subacute toxicity (28 days) and systemic chronic toxicity (40 days) studies were carried out in normal Swiss albino mice showed 1 is significantly nontoxic to the host.

Provided is a grease-producing yeast mutant strain which can be synchronously stopped in a specific cell cycle at which the grease yield is high by temperature change. The mutant strain is a lipomyces starkeyi strain which is pre-cultured at 23-26 DEG C and then formally cultured at 32-35 DEG C and is synchronously stopped in a G1 phase, or is a lipomyces starkeyi strain which is pre-cultured at 20-23 DEG C and then formally cultured at 30-32 DEG C and is synchronously stopped in a G2 / M phase.

The one or more embodiments of the specification provide a cell radiosensitivity determination method, comprising: adopting a preset cell cycle arrest method to process a plurality of cell test groups of target cells respectively, to obtain a plurality of cell test groups with different G1 phase proportions; wherein the G1 phase proportion is the proportion of cells in the G1 phase in the cell test group; performing a radiation operation on the plurality of cell test groups, and determining a cell biological index in each cell test group after the radiation operation; based on the G1 phase proportion of each cell test group and the corresponding cell biological index, constructing a data model for indicating the corresponding relationship between the G1 phase proportion and the cell biological index of the target cell, for evaluating the radiation sensitivity of the target cell.

A use of a phytic acid in the preparation of a reagent for relieving mitochondrial impairment. The phytic acid has the effects of improving the average volume, surface area and length of mitochondria, reducing a sphericity rate, reducing the ROS level, reducing DNA damage, improving a G1 phase ratio, promoting removal of damaged mitochondria in cells, recycling metabolites in the cells and the like.

The invention discloses application of pinoresinol in treatment of rectal cancer, it is found for the first time that the pinoresinol can inhibit expression of CaLM1, then CaLM1 / CaMKII / CREB signaling pathways can be inhibited by reducing expression levels of CAMKII and p-CREB, and on the basis of the inhibition of the expression levels of CAMKII and p-CREB, the application of the pinoresinol in treatment of rectal cancer is achieved. The pinoresinol is used as an inhibitor of a CaLM1 / CaMKII / CREB signal channel for the first time, in-vitro and in-vivo effects on rectal cancer cells and solid tumors thereof are experimented, and it is found that in-vitro pinoresinol dose dependence reduces expression of CaLM1, CaMKII and p-CREB, proliferation of cancer cells is remarkably inhibited, apoptosis of the cancer cells is promoted, and the tumor cell cycle is retarded in the G0 / G1 phase. In-vivo experiments show that the volume and weight of tumors are reduced by dosages of the pinoresinol, and the experiments find that the rectal cancer inhibition effect of the high-concentration pinoresinol (20.0 mg / kg) is close to that of a known chemotherapeutic drug cis-platinum (8.0 mg / kg) with a curative effect; in addition, the TUNEL experiment and the immunohistochemical analysis further support the apoptosis promoting and anti-proliferation effects of the pinoresinol by inhibiting the CaLM1 / CaMKII / CREB signal channel.

This invention relates to the application of (E)-2-(4-(dimethylamino)styryl)-6-methoxy-3-methylbenzo[d]thiazol-3-onthium in the preparation of anticancer drugs, belonging to the field of pharmaceutical technology. The structure of (E)-2-(4-(dimethylamino)styryl)-6-methoxy-3-methylbenzo[d]thiazol-3-onthium is shown in Formula I below. The (E)-2-(4-(dimethylamino)styryl)-6-methoxy-3-methylbenzo[d]thiazol-3-onthium of this invention can inhibit the growth of gastric cancer cells. By promoting autophagy and mitochondrial fragmentation in gastric cancer cells AGS and HGC-27, it inhibits the proliferation, invasion, and migration of gastric cancer cells and arrests them in the G1 phase. Furthermore, in vivo experiments in mice have confirmed that ZWK-3 can inhibit tumor growth in mice in a significant dose-dependent manner, without affecting mouse body weight or visceral indices. Formula I.