Ninjurin 2 rs118050317 gene polymorphism and endometrial cancer risk

Chen, Yimin; Yang, Liting; Shi, Guangyao; Chen, Peng; Li, Liang; Fang, Hangrong; Chen, Chao

doi:10.21203/rs.3.rs-35102/v1

Cited by 1 publication

(2 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…positively affects the progression of CRC and EMT formation through the regulation of miR-129-5p and DNMT3A [31]. Meanwhile, circPTPN22 inhibits the proliferation and metastasis of gastric cancer cells by inhibiting the EMT pathway through competitive miRNA binding [32]. To evaluate whether circ-SIRT1 knockdown affects EMT, thereby inhibiting cell migration and invasion, we measured the expression of EMT marker proteins in CRC cells depleted of circ-SIRT1.…”

Section: Discussionmentioning

confidence: 99%

“…The results showed that the expression of the EMT marker proteins N-cadherin and vimentin was decreased, while that of E-cadherin was increased, indicating that the loss of circ-SIRT1 expression can result in EMT inhibition. Several studies have reported on the interaction between circRNAs and proteins in tumors [32,33]. Here, we used the CircInteractome web tool to predict the proteins that could bind to circ-SIRT1 and selected the highest-ranked one, EIF4A3, for further investigation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

circ-SIRT1 Promotes Colorectal Cancer Proliferation and EMT by Recruiting and Binding to eIF4A3

Wang

Liu

et al. 2021

Analytical Cellular Pathology

View full text Add to dashboard Cite

Circular RNA (circRNA), a recently identified type of endogenous noncoding RNA, has been implicated in the occurrence and development of a variety of tumors; however, whether circ-SIRT1, derived from pre-mRNA of the parental SIRT1 gene, is involved in colorectal cancer (CRC) remains unknown, as do the potential underlying mechanisms. The expression of circ-SIRT1 in CRC cells and tissue was detected by RT-qPCR. Colony formation and Cell Counting Kit-8 assays were used to evaluate the effect of circ-SIRT1 knockdown on the proliferative ability of CRC cells. Wound healing and Transwell assays were used to assess the effect of circ-SIRT1 knockdown on the migratory and invasive capacity of CRC cells. RNA immunoprecipitation and RNA pull-down assays were employed to validate the binding of circ-SIRT1 to EIF4A3. Western blot was used to identify the changes in the expression of EIF4A3 and EMT-related proteins. The RT-qPCR results showed that circ-SIRT1 was highly expressed in CRC cells and tissue and was positively correlated with the depth of tumor invasion. Knocking down circ-SIRT1 inhibited the proliferation and invasion of CRC cells and EMT. We further found that EIF4A3 could bind to circ-SIRT1, and that overexpressing circ-SIRT1 decreased the abundance of EIF4A3 at the mRNAs of the EMT marker proteins N-cadherin and vimentin. Combined, our findings suggested that circ-SIRT1 regulates the expression of EMT-related proteins by preventing EIF4A3 recruitment to the respective mRNAs. Our results further indicate that circ-SIRT1 functions as an oncogene in CRC by promoting the proliferation, invasion, and EMT of CRC cells through the circ-SIRT1/EIF4A3/N-cadherin/vimentin pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%