scholarly journals MiR-6803-5p Promotes Cancer Cell Proliferation and Invasion via PTPRO/NF-κB Axis in Colorectal Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Shushan Yan ◽  
Min Cheng ◽  
Quanhong Duan ◽  
Zengfang Wang ◽  
Wenfeng Gao ◽  
...  

Accumulated studies have implicated microRNAs (miRNAs) exert modifying effects on colorectal cancer (CRC). Protein tyrosine phosphatase, receptor type O (PTPRO) has been identified as a tumor suppressor in several kinds of cancer, including CRC. Previously, we have found that exosome-encapsulated miR-6803-5p is increased in CRC. However, the mechanism of miR-6803-5p in CRC is not clear yet. This study is aimed at elucidating the effect of miR-6803-5p in colorectal carcinogenesis. Expression of miR-6803-5p and PTPRO mRNA in peripheral blood mononuclear cells of CRC patients is estimated by real-time PCR. PTPRO protein in CRC cells is detected by western blot. To verify the association of miR-6803-5p with PTPRO, luciferase reporter assay is performed. CCK-8 and EdU assays are conducted to assess cell proliferation. Real-time PCR and ELISA are applied to detect cytokine expression in CRC cells. Cell invasion and migration assays are evaluated by transwell and scratch tests. Immunofluorescence is carried out to determine the activation of NF-κB in HCT116 cells. Negative correlation is demonstrated between miR-6803-5p and PTPRO in CRC. PTPRO is demonstrated to be a direct target of miR-6803-5p. miR-6803-5p can promote cancer cell proliferation and invasion and enhance inflammation through PTPRO/NF-κB axis in CRC, which serves as a useful target for CRC.

2020 ◽  
Vol 10 (4) ◽  
pp. 518-524
Author(s):  
Feng Deng ◽  
Xiaoping Zhou ◽  
Yang Liu ◽  
Haiding Wang ◽  
Yinzi Li

Gastric cancer pathogenesis remains to be elucidated. LncRNAs involve in tumorigenesis. LncRNA SNHG15 is abnormally expressed in several tumors, but its role in gastric cancer is unclear. The tumor tissue and adjacent tissues of gastric cancer patients were collected for measuring LncRNA SNHG15 and miR-92a expressions by Real time PCR. Gastric cancer cell line SGC-7901 was divided into NC group, si-SNHG15 group, and si-UCA1+ miR-92a inhibitor group followed by analysis of cell proliferation by MTT assay, Capase-3 activity as well as Bax and Bcl-2 level by Real-time PCR. Gastric cancer tissues presented significantly increased LncRNA SNHG15 and decreased miR-92a expression than adjacent tissues (P < 0 05). LncRNA SNHG15 and miR-92a expression was associated with the tumor differentiation and pathological stage (P < 0 05) with a negative correlation between them. SNHG15 siRNA transfection significantly inhibited SNHG15 expression and tumor cell proliferation and invasion, increased Caspase 3 activity and Bax level, and decreased Bcl2 (P < 0 05). miR-92a was a targeted miRNA for LncRNA SNHG15. Addition of miR-92a inhibitor can significantly reverse the above changes (P < 0 05). LncRNA SNHG15 expression is increased and miR-92a expression is decreased in gastric cancer and correlated with the tumor pathological stage. LncRNA SNHG15 regulates human gastric cancer cell proliferation, apoptosis and invasion via targeting miR-92a.


2015 ◽  
Vol 46 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Wenming Wu ◽  
Qiao Wu ◽  
Xiafei Hong ◽  
Guangbing Xiong ◽  
Yi Xiao ◽  
...  

2021 ◽  
Author(s):  
Xuefeng Xing ◽  
Ming An ◽  
Tonghua Chen

Abstract Background Ovarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear. Objective The present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer. Methods The expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms. Results SNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells. Conclusions SNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.


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