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    Home > Active Ingredient News > Antitumor Therapy > Q1 Partition Cell Allus High is recommended by cited papers. The team revealed the molecular mechanisms by which lncRNA-SNHG7 promotes the development of lung cancer.

    Q1 Partition Cell Allus High is recommended by cited papers. The team revealed the molecular mechanisms by which lncRNA-SNHG7 promotes the development of lung cancer.

    • Last Update: 2020-07-18
    • Source: Internet
    • Author: User
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    Congratulations to cell promotion for its impact factor rising to 5.753 in the newly released Journal Citation Report 2020 (JCR) and entering cell biology Q1 partition! Competitive endogenous RNA (Cerna) is a mechanism of RNA to RNA interaction, which is mainly realized by miRNA response elements (MRes). MiRNA can combine with mRNA through MRE, leading to mRNA degradation or inhibiting its translation [1].in recent years, studies have found that MRE exists not only on mRNA, but also on other types of RNA such as long non coding RNA (lncrna), circular RNA (circrna), which means that the same miRNA can bind to many types of RNA, and there is a competitive relationship between RNA molecules that combine the same miRNA [2].when lncrna and mRNA have the same MRE, they form a competition relationship for the same miRNA. Lncrna indirectly regulates the mRNA expression level through the MRE bridge, thus regulating the cell function [3].< CEBR / > also plays an important role in the development of lung cancer.lung cancer is one of the most dangerous malignant tumors to people's health and life. Understanding the tumor biology and pathogenesis of non-small cell lung cancer will contribute to the targeted treatment of lung cancer.in January 2018, Professor He Jianxing from the First Affiliated Hospital of Guangzhou Medical University published the research results entitled "mir-193b availability is inhibited by lncrna ‐ snhg 7 for FAIM 2-induced tumour progress in non ‐ small cell lung cancer" in January 2018, which was firstly found in non-small cell lung cancer (NSCLC), In NSCLC, lncrna-snhg7 plays an important role in the development of NSCLC by competitive binding of mir-193b with Cerna mechanism.this original paper, published in the first issue of cell promotion in 2018, has been cited 63 times as of the time of publication according to the data base of korev web of science, which is a highly cited paper.previously, Professor He Jianxing's team published "lncrna-snhg7 promotes the promotion" in oncology reports, Migration and invasion and inhibitors apoptosis of lung cancer cells by enhancing the faim2 expression "revealed that lncrna-snhg7 can promote the proliferation, migration and invasion of lung cancer cells and inhibit their apoptosis by enhancing the expression of faim2 [4], but the possible molecular mechanism remains unclear.in this study, the expression levels of lncrna-snhg7 in NSCLC tissues and corresponding normal tissues were detected, and the results showed that the expression level of lncrna-snhg7 was positively correlated with lymph node metastasis and TNM stage of NSCLC, indicating that lncrna-snhg7 mainly plays a role of carcinogenic gene in NSCLC.in order to explore whether lncrna-snhg7 can act as Cerna, the researchers used bioinformatics and mirwalk to analyze, and found that there were lncrna-snhg7 and faim2 binding sites on mir-193b. Luciferase reporter gene experiments proved that mir-193b interacted with lncrna-snhg7 and faim2, and mir-193b could also regulate the expression of faim2.mir-193b has the same binding site with lncrna-snhg7 and faim2. The team further studied the interaction between lncrna-snhg7, mir-193b and faim2.using CCK-8, Transwell and flow cytometry, it was proved that faim2 can promote the proliferation, migration and invasion of A549 and h125 tumor cells, but overexpression of mir-193b can significantly inhibit the effect of faim2 and promote the apoptosis of tumor cells.in addition, overexpression of lncrna-snhg7 can restore the function of faim2 inhibited by mir-193b, which indicates that there is an antagonistic effect between lncrna-snhg7 and mir-193b.antagonism between lncrna-snhg7 and mir-193b in order to confirm the carcinogenic effect of lncrna-snhg7 in vivo, researchers injected lncrna-snhg7 knockdown or overexpressed conditional tumor cells into nude mice to establish xenotransplantation model.the results showed that lncrna-snhg7 could promote tumor growth, lncrna-snhg7 could inhibit mir-193b expression and up regulate faim2 expression in vivo.in addition, the expression of EMT related markers changed significantly in mice with lncrna-snhg7 overexpression, which indicated that lncrna-snhg7 could affect the occurrence and development of NSCLC by promoting EMT.in conclusion, this study found that lncrna-snhg7 can regulate the expression of faim2 through the mechanism of Cerna competitively combining with mir-193b, which reveals the molecular mechanism of lncrna-snhg7 affecting the occurrence and development of lung cancer, and provides new targets and ideas for the treatment of lung cancer. [2] Kataoka m, Wang D Z. non coding RNAs including miRNAs and lncrnas in cardiovascular biology and disease. Cells. 2014; 3 (3): 883-898. [3] Nie W, Ge h, J, J, J, J, J, J, J, J, J, J, J, J, J, J, J, Yaya, Yaya, Yaya, yayaya, Yaya, yayaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yaya, Yang x Q, sun x, Huang H, Tao X, Chen W S, Li B. Lncrna-uca1 exerts oncogenic functions in non-small cell lung cancer by targeting mir-193a-3p. Cancer Lett. 2016; 371(1):99-106.[4] She K, Huang J, Zhou H, Huang T, Chen G, He J. Lncrna-snhg7 promotes the proliferation, Migration and invasion and investments apoptosis of lung cancer cells by enhancing the faim2 expression. Oncol Rep. 2016; 36 (5): 2673-2680, He J. mir-193b availability is agonized by lncrna-snhg7 for faim2 induced tumour progression in non small cell lung cancer. Cell prolif. 2018; 51: e12406. Next, we will introduce other highly cited articles published on cell promotion for free reading. Welcome to your attention! About cell promotion cell promotion is a peer-reviewed open access (OA) Journal of cell biology. the frontier articles published by cell promotion are presented through strict and fair peer review process, and are presented with the highest quality production standards, so as to create the best quality open access journals. at present, cell proliferation is considered as the main reference in cancer and stem cell research. It publishes important research results related to cell proliferation and differentiation such as stem cells, cell aging, regenerative medicine, cell death, tissue engineering, etc. cell proliferation covers stem cells, regenerative medicine, tissue engineering, cell cycle control, cell aging, cell death, mathematical modeling, etc. author benefits! Open Access Journals: as soon as the papers are published, they can be downloaded and read free of charge, and the speed of peer review is fast: the average time from the author's contribution to the first decision of the editor is 11.1 days; the average time from the author's submission to the final decision of the editor is 17.6 days Editor Lin Yunfeng, associate editors Professor Fabio grizzi humanitas research hospital, Sichuan University, n. Shyh Chang, Institute of zoology, Chinese Academy of Sciences
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