Ophiopogonin-B Suppresses Epithelial-mesenchymal Transition in Human Lung Adenocarcinoma Cells via the Linc00668/miR-432-5p/EMT Axis

Hu, Cheng; Jiang, Rilei; Cheng, Zhen; Lu, Yueyang; Gu, Ling; Li, Hongxiao; Li, Liqiu; Gao, Qian; Chen, Meijuan; Xu, Zhonghua

doi:10.7150/jca.31338

Cited by 22 publications

(8 citation statements)

References 21 publications

(25 reference statements)

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“…More and more cancer-related lncRNAs have been identified recently. Many lncRNAs were proved to have effects on HCC progression, among which, LINC00668 was found to serve as an oncogene in several cancers such as colorectal cancer [25] and lung adenocarcinoma [26]. LncRNA LINC00668 was reported to accelerate progression of breast cancer [27].…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

2020

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Liver cancer is now one of the most lethal and commonest cancers in the world, among which over 90% is hepatocellular carcinoma (HCC). Recent studies have confirmed long non-coding RNAs (lncRNAs) are implicated in carcinogenesis. It has been reported lncRNA LINC00668 serves as an oncogene in several cancers. However, the mechanism where LINC00668 regulates HCC is still unclear. qRT-PCR analysis was adopted to detect the expression of relative RNAs. Cytoplasmic and nuclear RNA fraction analysis was conducted to verify the underlying molecular mechanism. Cell colony formation was carried out to test cell colony formation ability and transwell assays were performed to testify cell migratory and invaded abilities. Relevant protein expression level was measured by Western blot assay. LINC00668 was significantly up-regulated in HCC tissues and cell lines. LINC00668 knockdown inhibited cell proliferative, migratory and invasion abilities and slowed down the epithelial–mesenchymal transition (EMT) process. Mechanistically, LINC00668 positively modulates the expression of YY1 by competitively binding to miR-532-5p. It was revealed that LINC00668 up-regulation accelerated cell proliferation and motility in HCC and suggested LINC00668 could be a potential therapeutic target for HCC.

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Section: Discussionmentioning

confidence: 99%

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

2020

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“…It has also been reported that Linc00668, associating with the PRC2 complex, epigenetically silenced the cyclin-dependent protein kinase inhibitors (CKIs) and promoted cell proliferation in gastric cancer (16). Linc00668 also functioned as a ceRNA to promote tumor progression in several types of cancer (17,(51)(52)(53)(54). In this study we observed that Linc00668 promoted breast cancer cell invasion, stem-cell like capacity, and Dox resistance via its binding to SND1.…”

Section: Discussionmentioning

confidence: 63%

Linc00668 Promotes Invasion and Stem Cell-Like Properties of Breast Cancer Cells by Interaction With SND1

Qian

Zhu

et al. 2020

Front. Oncol.

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Long non-coding RNAs (lncRNAs) are reported to be involved in breast cancer progression. Herein, we observed that the expression of Linc00668 was increased in breast cancer compared to normal tissue. The patients with high Linc00668 expression exhibited an association with a higher metastatic risk. We demonstrated that forced expression of Linc00668 enhanced, whereas depletion of Linc00668 diminished invasion and self-renewal of breast cancer cells as well as resistance to doxorubicin (Dox). Further mechanistic studies revealed that Linc00668 associated with staphylococcal nuclease domain-containing 1 (SND1) and regulated the expression of downstream genes. Linc00668 depletion led to reduced expression of the downstream target of SND1 and further attenuated the self-renewal capacity of breast cancer cells. Our observations suggest that Linc00668 promotes metastasis, and chemotherapeutic resistance in breast cancer by interacting with SND1. Therefore, Linc00668 may serve as a potential therapeutic modulator in breast cancer treatment.

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“…The previous studies have demonstrated that miR-432-5p function in glioma [ 19 ], lung adenocarcinoma [ 20 ]. Given the fact that miR-432-5p has been proved to be related with NSCLC, sponged by lncRNA MSTRG.51053.2 or Linc00668 to affect the progression of NSCLC [ 21 , 22 ], we deciphered and studied the potential ceRNA relationship between LINC01783 and miR-432-5p.…”

Section: Discussionmentioning

confidence: 99%

LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway

2021

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Background Non-small cell lung cancer (NSCLC) is a common malignancy around the globe. Increasing long non-coding RNAs (lncRNAs) have been confirmed to be associated with the progression of cancers, including NSCLC. Long intergenic non-protein coding RNA 1783 (LINC01783) is a novel lncRNA and its regulatory function as competing endogenous RNA (ceRNA) has not been studied in NSCLC. Methods RT-qPCR measured the expression level of LINC01783 in NSCLC cells. CCK-8, EdU, transwell and wound healing assays were conducted to detect cell proliferation, migration and invasion in NSCLC. The relationship between miR-432-5p and LINC01783 along with delta like 1 (DLL-1) was illustrated by RNA pull down, RIP and luciferase reporter assays. Results LINC01783 was found remarkably increased in NSCLC cell lines, and down-regulation of LINC01783 suppressed cell proliferation, migration and invasion. Then, we discovered Notch pathway was related to the progression of NSCLC, and DLL-1 expression was reduced by LINC01783 knockdown. Furthermore, DLL-1 overexpression could counteract the suppressive effects of LINC01783 down-regulation on the growth of NSCLC cells. MiR-432-5p was observed to be the mutual miRNA that could bind with both LINC01783 and DLL-1. Overexpression of miR-432-5p inhibited DLL-1 expression. In the rescue assays, miR-432-5p depletion offset the impacts of LINC01783 knockdown, and then DLL-1 silence recovered the influence of miR-432-5p down-regulation on NSCLC cell growth. Conclusion LINC01783 aggravates NSCLC cell growth by regulating Notch pathway and sponging miR-432-5p, being a potential target in the treatment for NSCLC.

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Ophiopogonin-B Suppresses Epithelial-mesenchymal Transition in Human Lung Adenocarcinoma Cells via the Linc00668/miR-432-5p/EMT Axis

Cited by 22 publications

References 21 publications

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

Linc00668 Promotes Invasion and Stem Cell-Like Properties of Breast Cancer Cells by Interaction With SND1

LINC01783 facilitates cell proliferation, migration and invasion in non-small cell lung cancer by targeting miR-432-5p to activate the notch pathway

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