ABSTRACT
Methyltransferase-like 3 (METTL3), as the most important methylase of N6-methyladenine (m6A),plays an important role in the development and progression of breast cancer by influencing various regulatory mechanisms, such as methylation level, mRNA stability of cancer-related genes, oncogene expression and cancer cell signaling pathways. This paper reviews the regulatory mechanism of METTL3 in breast cancer and summarizes the latest research progress of METTL3 in the development and progression of breast cancer.
ABSTRACT
Objective: To evaluate the inhibition of human endostatin on tumor growth and metastasis of lung adenocarcinoma LA795 in mice. Methods: Recombinant human endostatin was purified from pCX expressed endostatin clones. Plasminogen was purified from outdated human plasma by affinity chromatography, and human angiostatin was produced from human plasminogen digested by elastase and purified by affinity chromatography. LA795 cells were inoculated subcutaneously into the dorsa of T739 mice, and the mice were randomized into 3 groups. From the 1Oth day, the first group was given 20 mg/kg of recombinant human endostatin s.c. qd, the second was treated daily s. c. of 7.5 mg/kg of human angiostatin, and the third group received daily s.c. with equal volumes of PBS for 14 days. Volumes of the subcutaneous tumors, lung weights, the number of lung surface metastases and mice life span were observed. The results were analyzed by q-test. Results: The tumor volumes of both the 1 st and the 2nd groups increased slowly. From the 8th day after being treated, the tumor volumes were decreasing. However, in the 3rd group, the tumor volumes increased continuously. The lung weight and the number of lung surface metastases of the 1st and 2nd groups were less than that of the 3rd group. The average survival periods of the 1st and 2nd groups were longer than that of the 3rd group. Conclusion: Human endostatin and angiostatin have strong inhibitory effects both on growth of primary tumor and metastasis of lung adenocarcinoma LA795, and prolongs the survival period of the tumor-bearing mice.
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Objective: To investigate the combined inhibitive effect of TNP-470 and rhES on the growth of lung adenocarcinoma LA795 in T739 mice. Methods: The purified rhES was acquired by using methanol to induce the recombinant pichia pastoris. GS115 and heparin affinity chromatography. The T739 mice inoculated with LA795 cells were randomized into three groups, 10 mice per group, one group was injected with PBS for 14 days, the other two groups were respectively treated with rhES and TNP-470+rhES. To observe the tumor growth in different groups, and the tumor volume was measured with caliper. The microvessel density(MVD) of tumors were measured by using immunohistochemistry. Results: The purified rhES was acquired. In compared with PBS group, the tumor growth of other two groups was inhibited significantly. And the tumor volume of TNP-470+rhES group are smaller than the rhES group (P
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AIM: To investigate whether leukotriene D 4(LTD 4) would stimulates proliferation of cultured human airway smooth muscle (ASMC). METHOD: Human ASMC were isolated and subcultured, varying concentration of LTD 4 were added to the media. Cell counts were obtained, [3H]-thymidine([3H]-TdR) incorporation and inositol 1, 4, 5-trisphosphate (IP 3) accumulation were measured. RESULTS: LTD 4(0.1 nmol?L -1～10 nmol?L -1) increased cell number and also increased incorporation of [3H]-TdR and accumulation of IP 3 in a concentration dependent manner(P