Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway

Zhou, Jianping; Zhi, Xiaofei; Wang, Linjun; Wang, Weizhi; Li, Zheng; Tang, Jie; Wang, Jiwei; Zhang, Qun; Xu, Zekuan

doi:10.1186/s13046-015-0250-6

Cited by 112 publications

(126 citation statements)

References 21 publications

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“…We observed that high expression level of EGFR-AS1 in GC patients was significantly correlated with tumor size, but no significant correlation between EGFR-AS1 expression and other clinicopathological features were These data suggest that EGFR-AS1 serves as an oncogenic lncRNA in gastric cancer. The expression of EGFR in clinical samples was found to be significantly higher in GC tissues than in adjacent non-tumor tissues, which is consistent with other reports [31]. Also, a significantly positive correlation was observed between the expression of EGFR and EGFR-AS1.…”

Section: Discussionsupporting

confidence: 81%

Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer

Qian

Peng

et al. 2018

Cell Physiol Biochem

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Background/Aims: LncRNA EGFR-AS1 is an antisense transcript of EGFR, which plays a key role in gastric cancer progression. This study was aimed to explore the effects of lncRNA EGFR-AS1 on GC and the underling mechanisms. Methods: The silencing of EGFR-AS1 expression was performed by using EGFR-AS1 shRNA lentivirus in MGC803 and SGC-7901 GC cell. The levels of lncRNA EGFR-AS1 and EGFR were detected by qPCR and western blot. Cell proliferation was assessed by CCK-8, EdU, and colony formation assays. The EGFR mRNA stability was explored by using RNA synthesis inhibitor α-amanitin. Results: In our study, EGFR-AS1 significantly up-regulated in GC tissues and correlated with tumor size. And the expression of EGFR-AS1 positively correlated with EGFR in tissues. Moreover, knock-down of EGFR-AS1 inhibited the proliferation of GC cells via suppressing EGFR-dependent PI3K/AKT pathway in vitro and in vivo. Mechanismly, depletion of EGFR-AS1 was found to decrease EGFR expression by reduction of EGFR mRNA stability. Conclusion: Our findings suggested that EGFR-AS1 might have an oncogenic effect on GC and serve as a potential target of GC.

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Section: Discussionsupporting

confidence: 81%

Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer

Qian

Peng

et al. 2018

Cell Physiol Biochem

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“…Previously published studies have revealed that the knockdown of linc00152 could inhibit cell proliferation and suppress cell cycle progression [22, 37, 38]. In our study, we obtained similar results to such studies.…”

Section: Discussionsupporting

confidence: 82%

Long Noncoding RNA Linc00152 Functions as a Tumor Propellant in Pan-Cancer

Wan

Yin

et al. 2017

Cell Physiol Biochem

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Background/Aims: The oncogenic role of linc00152 in pan-cancer is unclear. Methods: In this study, RNA-Seq of 33 breast specimens was performed, and the expression of linc00152 was validated by qPCR using 50 paired breast cancer tissues and adjacent normal tissues. This result combined with the expression of linc00152 in pan-cancer was revalidated by Gene Expression Omnibus and The Cancer Genome Atlas data. Next, the oncogenic roles of linc00152 in view of prognosis, chemoresistance, genomic and epigenetic regulation, including DNA methylation and histone modification, potential biological function enrichment, and basic molecular function in pan-cancer, were also evaluated in vitro and in vivo. Results: Linc00152 is upregulated in pan-cancer, especially in progressive cancer, and the high expression of linc00152 may lead to a worse prognosis and chemoresistance in pan-cancer patients. Amplification, DNA hypomethylation, promoter-like lncRNA characteristics and super-enhancer regulation are the drivers that lead to the upregulation of linc00152 in pan-cancer. Meanwhile, linc00152 was involved in cancer-related pathways, infection and immune response-associated pathways by enriched analysis using TCGA data. Finally, linc00152 was confirmed to promote the proliferation, migration and invasion in MDA-MB-231, SGC-7901 and 786-O. Moreover, RIP and RNA pull-down assays indicated that linc00152 can bind to EZH2 directly. Conclusion: All of the results indicated that linc00152 acted as an oncogenic propellant from various perspectives, and it may be an effective therapy target in pan-cancer.

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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: 69%

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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Linc00152 promotes proliferation in gastric cancer through the EGFR-dependent pathway

Cited by 112 publications

References 21 publications

Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer

Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer

Long Noncoding RNA Linc00152 Functions as a Tumor Propellant in Pan-Cancer

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

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