Long non-coding RNA Linc00152 is involved in cell cycle arrest, apoptosis, epithelial to mesenchymal transition, cell migration and invasion in gastric cancer

Zhao, Jing; Liu, Yongchao; Zhang, Wenhong; Zhou, Zhongwen; Wu, Jing; Cui, Peng; Zhang, Ying; Huang, Guangjian

doi:10.1080/15384101.2015.1078034

Cited by 210 publications

(218 citation statements)

References 39 publications

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“…As a novel LncRNA, Linc00152 is increased in several cancers and exerts multiple functions to influence the tumor progression. [26][27][28] In this study, we report for the first time that Linc00152 promotes L-OHP resistance in colon cancer cells in vitro and in vivo. Mechanistically, Linc00152 confers resistance to L-OHP by competitively binding miR-193a-3p, upregulating ERBB4, and then inducing the activation of AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 68%

Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer

et al. 2016

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Long noncoding RNAs act as crucial regulators in plenty of human cancers, yet their potential roles and molecular mechanisms in chemoresistance are poorly understood. This study showed that a novel lncRNA, long intergenic noncoding RNA 152 (Linc00152 ), promoted tumor progression and conferred resistance to oxaliplatin (L-OHP)-induced apoptosis in vitro and in vivo. It antagonized chemosensitivity through acting as a competing endogenous RNA to modulate the expression of miR-193a-3p, and then erb-b2 receptor tyrosine kinase 4 (ERBB4). Knockdown of ERBB4 in colon cancer cells decreased AKT phosphorylation, which resulted in decreased L-OHP resistance. Consistent with above findings, the specific AKT signaling inhibitor and activator were used, respectively, which demonstrated that Linc00152 contributed to L-OHP resistance at least partly through activating AKT pathway. Further studies indicated that Linc00152 was increased and appeared to be an independent prognostic factor for decreased survival and increased disease recurrence in stage II and III colon cancer patients undergoing L-OHP-based chemotherapy after surgery. Collectively, our findings established Linc00152 as a candidate prognostic indicator of outcome and drug responsiveness in colon cancer patients, and the involvement of competing endogenous RNAs mechanism in Linc00152/ miR-193a-3p/ERBB4/AKT signaling axis may provide a novel choice in the investigation of drug resistance.

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Section: Discussionmentioning

confidence: 68%

Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer

et al. 2016

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“…LncRNAs have been shown to influence a number of cellular functions, such as cell proliferation, migration, invasion, and apoptosis, by modulating gene expression at transcriptional and posttranscriptional levels [4-7]. Recently, Zhao et al have performed a lncRNA microarray analysis of gastric tumors and found 3141 lncRNAs which were significantly differentially expressed in tumor tissue compared to the paired normal gastric tissue [8]. It has been reported that H19, a 2.3-kb lncRNA which is transcribed from H19/Igf2 gene cluster located on human chromosome 11p15.5, is among the strongly upregulated lncRNAs [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway

Yan¹,

Zhang²,

Qiang³

et al. 2017

Cell Physiol Biochem

108

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Background: Long noncoding RNA (lncRNA) H19 is emerging as a vital regulatory molecule in the progression of different types of cancer and miR-675 is reported to be embedded in H19's first exon. However, their function and specific mechanisms of action have not been fully elucidated. The aim of this study was to identify a novel lncRNA-microRNA-mRNA functional network in gastric cancer. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the relative expression of H19 and miR-675 in normal (GES-1) and gastric cancer cell lines (SGC-7901, SGC-7901/DDP) as well as in tumor tissues. Gain and loss of function approaches were carried out to investigate the potential roles of H19/miR-675 in cell proliferation and apoptosis. Moreover, Fas associated via death domain (FADD) was validated to be the target of miR-675 via luciferase reporter assay. Western blotting was used to evaluate the protein expression of related signaling pathway. Results: In our study H19 and miR-675 were increased in gastric cancer cell lines and tissues. Overexpression of H19 and miR-675 promoted cell proliferation and inhibited cell apoptosis, whereas knockdown of H19 and miR-675 inhibited these effects. By further examining the underlying mechanism, we showed that H19/miR-675 axis inhibited expression of FADD. FADD downregulation subsequently inhibited the caspase cleavage cascades including caspase 8 and caspase 3. Conclusion: Taken together, our results point to a novel regulatory pathway H19/miR-675/ FADD/caspase 8/caspase 3 in gastric cancer which may be potential target for cancer therapy.

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“…For example, in lung cancer cells, upregulation of the lncRNA HOX transcript antisense RNA (HOTAIR) enhances cell proliferation, migration and invasion (8). In gastric cancer, the lncRNA Linc00152 is involved in cell cycle arrest, migration, invasion, apoptosis and the epithelial to mesenchymal (ETM) transition of cancer cells (9). Similarly, the lncRNA Linc00617 has been found to have oncogenic activity in breast cancer (10).…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA MALAT1 is upregulated and involved in cell proliferation, migration and apoptosis in ovarian cancer

Wang

Guo

2017

Experimental and Therapeutic Medicine

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Abstract. Ovarian cancer (OC) is the leading cause of mortality among gynecological malignancies. Although microRNAs are known to have a key regulatory role in OC, the involvement of long non-coding RNAs in the disease is less established. Previous studies have demonstrated that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a tumor oncogene in many cancers, though its role in OC remains unclear. The present study reported that MALAT1 expression was markedly upregulated in OC, by knockdown of MALAT1 expression in vivo, using RNA interference (RNAi) with small-interfering RNA (siRNA). It was found that MALAT1 expression was positively correlated with the International Federation of Gynecology and Obstetrics stages of OC, tumor histological grade and lymph node metastasis. In addition, the differential MALAT1 levels between a human ovarian epithelial cell line (HOSE) and OC cell lines (ES-2, OVCAR3, SKOV3 and HO8910) were compared in vitro. Notably, MALAT1 was expressed to a high level in OC cells. Furthermore, exogenous knockdown of MALAT1 significantly repressed growth and migration of OC cells, and promoted their apoptosis. Collectively, the current findings suggest that upregulation of MALAT1 in OC may facilitate tumorigenesis and metastasis. Knockdown of MALAT1 expression has potential as a novel target for the diagnosis and therapy of OC.

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Long non-coding RNA Linc00152 is involved in cell cycle arrest, apoptosis, epithelial to mesenchymal transition, cell migration and invasion in gastric cancer

Cited by 210 publications

References 39 publications

Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer

Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway

Long non-coding RNA MALAT1 is upregulated and involved in cell proliferation, migration and apoptosis in ovarian cancer

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