LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung cancer cells<i>via</i>regulating the miR-214/TRIM16 axis

Li, Qian; Chen, Kai; Dong, Rong; Lu, Haojie

doi:10.1039/c8ra09573f

Cited by 9 publications

(7 citation statements)

References 37 publications

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“…RNA Pull-Down Assay. RNA pull-down assay was executed as previously described [25]. In a word, BCa cells (1 × 10 7 ) were treated with biotinylated MIR4435-2HG probe (Sigma-Aldrich, St. Louis, MO), followed by addition of magnetic beads (Millipore, Bedford, MA).…”

Section: Transwell Assaymentioning

confidence: 99%

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[Retracted] lncRNA MIR4435‐2HG Accelerates the Development of Bladder Cancer through Enhancing IQGAP3 and CDCA5 Expression

Yang

Wang

et al. 2022

BioMed Research International

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Background. Bladder cancer (BCa) is one of the most prevalent cancers occurring in the urinary system. Long noncoding RNAs (lncRNAs), in recent years, have emerged as crucial regulators in various biological processes of tumors. Aim. To identify the role of MIR4435-2 host gene (MIR4435-2HG) and uncover its molecular mechanism in BCa. Methods. Firstly, quantitative real-time PCR (RT-qPCR) analysis was used to examine MIR4435-2HG expression in BCa cells. Cell Counting Kit-8 (CCK-8), 5-ethynyl-2 ′ -deoxyuridine (EdU), wound healing, and transwell assays were implemented to identify the role of MIR4435-2HG in BCa. RNA-binding protein immunoprecipitation (RIP), RNA pull down, and luciferase reporter assays were applied to explore the potential mechanism of MIR4435-2HG in BCa. Results. MIR4435-2HG was highly expressed in BCa. Moreover, MIR4435-2HG silencing abrogated BCa cell proliferation, migration, and invasion. In terms of underlying mechanism, MIR44352HG acted as a microRNA-2467-3p (miR-2467-3p) sponge to control the expression of IQ motif containing GTPase activating protein 3 (IQGAP3) and cell division cycle associated 5 (CDCA5), resulting in activation of the rat sarcoma virus (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) and PI3K/AKT/mTOR signaling pathways. Conclusion. MIR4435-2HG involves in the progression of BCa, which might provide novel insights for BCa treatment.

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Section: Transwell Assaymentioning

confidence: 99%

“…Eventually, dual-luciferase reporter assay system (Promega) was applied to detect the luciferase activity. Luciferase reporter assay was conducted and analyzed as previously described [25]. The experiment was executed in triplicate.…”

Section: Transwell Assaymentioning

confidence: 99%

[Retracted] lncRNA MIR4435‐2HG Accelerates the Development of Bladder Cancer through Enhancing IQGAP3 and CDCA5 Expression

Yang

Wang

et al. 2022

BioMed Research International

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“…For instance, the lncRNA BLACAT1 promoted ATG7 expression through miR-17, facilitated autophagy, and promoted the chemoresistance of NSCLC cells through the miR-17/ATG7 axis ( Huang et al, 2019 ). lncRNA CASC2 inhibited autophagy and promoted apoptosis in NSCLC cells via the miR-214/TRIM16 signaling pathway ( Li et al, 2018a ). LncRNA MSTO2P promotes lung cancer cell proliferation and autophagy by upregulating EZH2 ( Wang et al, 2019 ).…”

Section: Discussionunclassified

Identification of an autophagy-related 12-lncRNA signature and evaluation of NFYC-AS1 as a pro-cancer factor in lung adenocarcinoma

Tong

et al. 2022

Front. Genet.

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Objective: To develop an autophagy-related lncRNA-based risk signature and corresponding nomogram to predict overall survival (OS) for LUAD patients and investigate the possible meaning of screened factors.Methods: Differentially expressed lncRNAs and autophagy genes were screened between normal and LUAD tumor samples from the TCGA LUAD dataset. Univariate and multivariate Cox regression analyses were performed to construct the lncRNA-based risk signature and nomogram incorporating clinical information. Then, the accuracy and sensitivity were confirmed by the AUC of ROC curves in both training and validation cohorts. qPCR, immunoblot, shRNA, and ectopic expression were used to verify the positive regulation of NFYC-AS1 on BIRC6. CCK-8, immunofluorescence, and flow cytometry were used to confirm the influence of NFYC-AS1 on cell proliferation, autophagy, and apoptosis via BIRC6.Results: A 12-lncRNA risk signature and a nomogram combining related clinical information were constructed. Furthermore, the abnormal increase of NFYC-AS1 may promote LUAD progression through the autophagy-related gene BIRC6.Conclusion: 12-lncRNA signature may function as a predictive marker for LUAD patients, and NFYC-AS1 along with BIRC6 may function as carcinogenic factors in a combinatorial manner.

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“…These findings are in agreement with several other studies wherein lncRNAs have been shown to trigger apoptosis or autophagy in human cancer cells. For example, lncRNA CASC2 overexpression suppressed the proliferation of human hepatocellular cancer and lung cancer cells by triggering apoptotic cell death [ 23 , 24 ]. In yet another study, lncRNA CCAT2 induced autophagy in human gastric cancer cells [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA PTCSC3 inhibits human oral cancer cell proliferation by inducing apoptosis and autophagy

et al. 2021

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IntroductionLong non-coding RNAs (lncRNAs) have gained increased attention due to the discovery of their roles in cancer-related processes. LncRNA PTCSC3 has been shown to have tumour-suppressive effects in thyroid cancer and glioblastoma. This study investigated the role of lncRNA PTSC3 in human oral cancer.Material and methodsCell viability was determined by MTT assay. The induction of apoptosis was confirmed by 4,6-diamidino-2-phenylindole (DAPI) and Annexin V/PI assays. Ultrastructural analysis was performed by electron microscopy. Transwell assay was used to monitor the invasion of oral cancer cells.ResultsThe results revealed significant (p < 0.05) suppression of PTCSC3 expression in human oral cancer tissues and cell lines. The overexpression of PTCSC3 caused a significant (p < 0.05) decline in the proliferation of the human oral cancer cells via induction of apoptotic cell death which was accompanied by remarkable enhancement of Bax and suppression of Bcl-2. The electron microscopic analysis showed the development of autophagic vesicles in both the SCC-1 and SCC-9 cells indicative of autophagy. The western blotting analysis showed that PTCSC3 overexpression caused a remarkable increase in LC3B-I and Beclin 1 expression. PTCSC3 overexpression caused a significant (p < 0.05) decrease in invasion of the human SCC-1 and SCC-9 oral cancer cells. The invasion of the SCC-1 and SCC-9 cells was inhibited by 62% and 69% respectively.ConclusionsOverall, the evidence suggests that lncRNA PTCSC3 acts as a tumour suppressor in human oral cancer and suppresses oral cancer proliferation via induction of apoptosis and autophagy.

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LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung cancer cellsviaregulating the miR-214/TRIM16 axis

Abstract: Dysregulated long noncoding RNAs (lncRNAs) have been frequently observed in various cancers including non-small cell lung cancer (NSCLC) and are closely associated with cancer progression.

Cited by 9 publications

References 37 publications

[Retracted] lncRNA MIR4435‐2HG Accelerates the Development of Bladder Cancer through Enhancing IQGAP3 and CDCA5 Expression

[Retracted] lncRNA MIR4435‐2HG Accelerates the Development of Bladder Cancer through Enhancing IQGAP3 and CDCA5 Expression

Identification of an autophagy-related 12-lncRNA signature and evaluation of NFYC-AS1 as a pro-cancer factor in lung adenocarcinoma

Long non-coding RNA PTCSC3 inhibits human oral cancer cell proliferation by inducing apoptosis and autophagy

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