RETRACTED ARTICLE: Long non-coding RNA GAS5 sensitizes renal cell carcinoma to sorafenib via miR-21/SOX5 pathway

Liu, Lei; Pang, Xinlu; Wen-jin, Shang; Xie, Hongsheng; Feng, Yue; Gao, Feng

doi:10.1080/15384101.2018.1475826

Cited by 48 publications

(29 citation statements)

References 26 publications

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“…miR-21 can downregulate the Cdc25A, change the negative regulation of the G1/S phase of the cell cycle, and involve in DNA damage repair G2/M check the 19 point [31]. Numerous researches have shown that LncRNA GAS5 acts as a tumor suppressor in many types of malignancies by regulating the miR-21 [32][33][34][35]. In our research, we found overexpression of GAS5 reduced the resistance of drug and increased the apoptosis of gastric cancer cells.…”

Section: Discussionsupporting

confidence: 49%

The Long Noncoding RNA, Growth Arrest-Specific 5, Suppresses Gastric Cancer by Downregulating miR-21 Expression

Peng

Wang

et al. 2020

Pharmacology

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Background: Gastric cancer has become the second major cause of cancer death. The aim of the present study was to explore the relationship between miR-21 and the long noncoding RNA growth arrest-specific 5 (GAS5) in gastric cancer and the effect on gastric cancer cells. Methods: The expression of miR-21 and GAS5 mRNA was analyzed by quantitative real-time-PCR. Overexpression of GAS5 was used to investigate the biological functions of GAS5 in cells. The cell proliferation was detected by cell counting kit-8 assay and the cell migration and invasion were detected by Transwell. Cell apoptosis was evaluated by Annexin V-FITC/PI staining and apoptosis-related proteins were detected by western blot. The mechanism of GAS5 in vivo was evaluated by the tumorigenesis of nude mice, and dual luciferase reporter was used to determine if miR-21 is a GAS5 target. The inhibition of miR-21 and the simultaneous overexpression of GAS5 and miR-21 were further performed, and the above indicators were detected again. Results: GAS5 was low expression and miR-21 was high expression in gastric cancer tissues and cells. GAS5 overexpression reduced the proliferation, migration, and invasion of gastric cancer cells and increased the apoptosis of gastric cancer cells. The growth rate of GAS5 group slowed down and the volume of tumor decreased. miR-21 is a GAS5 target and GAS5 inhibits the proliferation of gastric cancer cells by targeting miR-21. Conclusion: Our research shown that overexpression of GAS5 can significantly inhibit the proliferation, migration, invasion and tumor formation of gastric cancer cells, and promote the apoptosis of gastric cancer cells, which may be related to the targeting inhibition of miR-21 expression by GAS5.

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Section: Discussionsupporting

confidence: 49%

The Long Noncoding RNA, Growth Arrest-Specific 5, Suppresses Gastric Cancer by Downregulating miR-21 Expression

Peng

Wang

et al. 2020

Pharmacology

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“…34 Moreover, GAS5 overexpression conferred sorafenib sensitive to RCC through miR-21/sex-determining region Y-box protein 5 (SOX5) regulatory pathway, suggesting that GAS5 could be a potential therapeutic target for sorafenib treatment in RCC. 135 Functionally, overexpression of GAS5 reduced viability and induced apoptosis via interacting with E2F transcription factor 4 (E2F4) and recruiting to enhancer of zeste homolog 2 (EZH2) promoter, which further repressed EZH2 transcription in T24 and EJ BCa cells. 93 GAS5 suppressed proliferation and induced cell cycle arrest via suppressing chemokine ligand 1 (CCL1) expression 136 and regulating CDK6 in BCa cells.…”

Section: Molecular Mechanismsmentioning

confidence: 99%

<p>Novel Tumor Suppressor lncRNA Growth Arrest-Specific 5 (GAS5) In Human Cancer</p>

Yu¹,

Hann²

2019

OTT

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Long noncoding RNAs (lncRNAs) play crucial regulatory roles in fundamental biological processes, and deregulations of lncRNAs have been linked to numerous human diseases, especially cancers. Of particular interest in this regard is lncRNA GAS5, which is mainly identified as a tumor suppressor in several cancers. GAS5 was significantly low expressed in multiple cancers and was associated with clinic-pathological characteristics and patient survival, indicating a novel potential diagnostic and prognostic biomarker, and a therapeutic target for cancer. Functionally, GAS5 is involved in cell proliferation, metastasis, invasion, apoptosis, epithelial-mesenchymal transition (EMT), and drug resistance, among others, via multiple molecular mechanisms, such as binding to DNA sequences, forming RNA-DNA triplex complex, triggering or suppressing the expression of genes, binding proteins to form chromatin-modifying complex, which activates or represses gene expression, and acting as miRNA sponge to suppress miRNA expression, leading to regulation of miRNA target genes. This review provides an overview of the current state of knowledge and role of GAS5 in clinical relevance, biological functions and molecular mechanisms underlying the dysregulation of expression and function of GAS5 in cancer. Finally, the potential prospective role as diagnostic and prognostic biomarker and therapeutic target in cancer is discussed.

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“…This is further considered in the slowest dividing cells in the body as opposed to its lowest levels in other rapidly dividing cells, the most important of which are cancer cells (25). GAS5 performs a tumor-suppressor role in human cancer (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). However, separate studies have indicated that GAS5 promotes proliferation, migration and invasion in esophageal cancer and hepatocellular carcinoma (26,27).…”

Section: Discussionmentioning

confidence: 99%

“…The gene consists of 12 exons and 11 introns from which 29 transcripts are produced from alternative splicing, many of which contain retained introns (4). Several studies have shown that GAS5 has a critical tumor-suppressive effect during progression of prostate cancer, renal cancer, ovarian cancer, cervical cancer as well as CRC (5)(6)(7)(8)(9)(10). Additionally, accumulating evidence has confirmed that GAS5 binds to microRNAs (miRs), such as miR-21, miR-196A, miR-205, miR-222 and miR-103, sponging their inhibitory effect on the target genes to perform tumor-suppressive roles (5,(11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

lncRNA GAS5 inhibits malignant progression by regulating macroautophagy and forms a negative feedback regulatory loop with the miR‑34a/mTOR/SIRT1 pathway in colorectal cancer

Zhang

Wang

et al. 2020

Oncol Rep

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Long non-coding RNA growth arrest specific 5 (GAS5) exerts inhibitory effects through the modulation of several target microRNAs (miRs) in cancer. However, its potential roles and underlying relationship during colorectal cancer (CRC) progression are unclear. Therefore, we explored the role of the negative feedback loop formed by the GAS5/miR-34a axis and mammalian target of rapamycin/sirtuin 1 (mTOR/SIRT1) pathway on macroautophagy and apoptosis in CRC. Expression of GAS5, miR-34a, SIRT1 and mTOR in CRC patients and cell lines was detected by quantitative reverse transcription polymerase chain reaction. Online bioinformatic analysis was used to predict the downstream miRs of GAS5. Luciferase assay and western blotting were performed to demonstrate miR-34a as a downstream target gene of GAS5 in CRC cells. The effects of the GAS5/miR-34a axis on apoptosis, macroautophagy, and the mTOR/SIRT1 pathway were assessed by flow cytometry, transmission electron microscopy and western blotting, respectively. Our results suggested that GAS5 was downregulated and acted as a molecular sponge of miR-34a during CRC progression. miR-34a participated in regulating GAS5-suppressed CRC cell macroautophagy and induced apoptosis through the mTOR/SIRT1 pathway. GAS5-mediated macroautophagy was maintained in an equilibrium state that might have a protective effect on CRC cell apoptosis. The mTOR signaling pathway suppressed GAS5 expression and formed a negative regulation feedback loop with miR-34a in CRC cells. Our results suggested that the GAS5/miR-34a/SIRT1/mTOR negative regulatory feedback loop mediated CRC cell macroautophagy, and maintained the cells in an autonomous equilibrium state, but not excessive activation state, which functions as a strong antiapoptotic phenotype during human CRC progression.

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RETRACTED ARTICLE: Long non-coding RNA GAS5 sensitizes renal cell carcinoma to sorafenib via miR-21/SOX5 pathway

Cited by 48 publications

References 26 publications

The Long Noncoding RNA, Growth Arrest-Specific 5, Suppresses Gastric Cancer by Downregulating miR-21 Expression

The Long Noncoding RNA, Growth Arrest-Specific 5, Suppresses Gastric Cancer by Downregulating miR-21 Expression

<p>Novel Tumor Suppressor lncRNA Growth Arrest-Specific 5 (GAS5) In Human Cancer</p>

lncRNA GAS5 inhibits malignant progression by regulating macroautophagy and forms a negative feedback regulatory loop with the miR‑34a/mTOR/SIRT1 pathway in colorectal cancer

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