10 results about "G1/S checkpoint" 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.

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 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.

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 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 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.