Long non-coding RNA LINC00115 contributes to the progression of colorectal cancer by targeting miR-489-3p via PI3K/AKT/mTOR pathway

Feng, Weiyu; Li, Baodong; Wang, Jinbang; Zhang, Huiliang; Liu, Yonggang; Xu, Dongli; Cheng, Ke; Zhuang, Jing

doi:10.21203/rs.3.rs-45664/v1

Cited by 1 publication

(1 citation statement)

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“…Molecular mechanism studies show that LINC00115 promotes breast cancer metastasis by regulating miR-7 and KLF4 expression. In colorectal cancer, LINC00115 inhibits the PI3K/AKT/mTOR signaling pathway by downregulating miR-489-3p, highlighting the LINC00115/miR-489-3p axis as a potential therapeutic target for colorectal cancer metastasis (18). So anti-LINC00115 compounds or agents consequently targeting the PI3K/AKT/mTOR pathway might serve as novel therapeutic strategies for the colorectal cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of LINC00115 inhibits the proliferation and invasion of lung cancer cells in vitro and in vitro

Shao¹,

Yu²,

Lü³

et al. 2021

Ann Transl Med

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Background: Lung cancer is a common malignant tumor in clinical practice. Its morbidity and mortality rank first among malignant tumors. However, the pathogenesis of lung cancer has not been fully clarified.This study found that LINC00115 is highly expressed in lung cancer tissues, but the role and molecular mechanisms of LINC00115 in the occurrence and progression of lung cancer are still unclear.Methods: Fluorescence quantitative PCR was used to detect the expression of LINC00115 in lung cancer tissues and para-carcinoma tissues. Cell counting kit-8 (CCK-8), clone formation, and Transwell assays were used to detect the effects of LINC00115 knockdown on the proliferation, clone formation, invasion, and migration of lung cancer cells. Western blot was used to detect the effects of LINC00115 knockdown on the expression of epithelial-mesenchymal transition (EMT)-related molecules. Finally, a xenograft model in nude mice was used to detect the effect of LINC00115 knockdown on the proliferation of lung cancer cells in vivo.Results: Compared with para-carcinoma tissue, LINC00115 was highly expressed in lung cancer tissue. Cell function experiments showed that knockdown of LINC00115 could significantly inhibit the proliferation, invasion, and migration of lung cancer cells. Western blot results showed that knockdown of LINC00115 could significantly inhibit the expression of the EMT-related proteins N-cadherin, vimentin, and fibronectin, and promoted the expression of E-cadherin. In vivo experiments in nude mice showed that knockdown of LINC00115 could significantly inhibit the proliferation of lung cancer tissues in vivo.Conclusions: LINC00115 is highly expressed in lung cancer tissues, and knockdown of LINC00115 can significantly inhibit the proliferation and invasion of lung cancer, which provides a theoretical basis for the design of targeted molecules for the subsequent treatment of lung cancer.

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Section: Introductionmentioning

confidence: 99%