PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2

Li, Hui; Ma, Xuhui; Yang, Dongyuan; Suo, Zhimin; Dai, Rujiang; Liu, Chunhong

doi:10.1002/jcb.29370

Cited by 40 publications

(21 citation statements)

References 33 publications

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“…Enhancer zeste homolog 2 (EZH2), catalytic subunit of polycomb complex 2 (PRC2), which interacts with LINC00152 in lung adenocarcinoma [20] and the promotion of DNA methylation in ESCC cells by non-coding RNA POU3F3 [21], have drawn much attention in recent years due to their involvement in the development of human diseases, such as [22] lung cancer [23], gastric cancer [24], breast cancer [25], T-cell acute lymphoblastic leukemia [26], and pediatric soft tissue sarcomas [27]. Herein, we hypothesize that LINC00152 might also interact with EZH2 in EC cells.…”

mentioning

confidence: 99%

LINC00152 upregulates ZEB1 expression and enhances epithelial-mesenchymal transition and oxaliplatin resistance in esophageal cancer by interacting with EZH2

Zhang

Liao

et al. 2020

Cancer Cell Int

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Background Expression of the long non-coding mRNA LINC00152 has been reported to correlate with cancer cell resistance to oxaliplatin (L-OHP). However, little is known regarding the molecular mechanism of LINC00152 in esophageal cancer (EC). Hence, we intended to characterize the role of LINC00152 in EC, with a special focus on epithelial-mesenchymal transition (EMT) and L-OHP resistance. Methods We collected EC tissues and identified EC cell lines with higher L-OHP resistance, and then characterized expression patterns of LINC00152, Zeste Homologue 2 (EZH2), Zinc finger e-box binding homeobox (ZEB1) and EMT-related genes using RT-qPCR and Western blot analysis. Furthermore, their functional significance was identified by gain and loss-of-function experiments. The relationship among LINC00152, EZH2 and ZEB1 was examined using RIP, RNA pull-down and ChIP assays. Additionally, resistance of EC cells to L-OHP was reflected by CCK-8 assay to detect cell viability. Animal experiments were also conducted to detect the effects of the LINC00152/EZH2/ZEB1 on EMT and L-OHP resistance. Results LINC00152, EZH2 and ZEB1 were highly expressed in EC tissues and Kyse−150/TE-1 cells. As revealed by assays in vitro and in vivo, LINC00152 positively regulated ZEB1 expression through interaction with EZH2 to enhance EMT and L-OHP resistance in EC cells. In contrast, silencing of LINC00152 contributed to attenuated EMT and drug resistance of EC cells to L-OHP. Conclusions Our study demonstrates that LINC00152/EZH2/ZEB1 axis can regulate EMT and resistance of EC cells to L-OHP, thus presenting a potential therapeutic target for EC treatment.

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mentioning

confidence: 99%

LINC00152 upregulates ZEB1 expression and enhances epithelial-mesenchymal transition and oxaliplatin resistance in esophageal cancer by interacting with EZH2

Zhang

Liao

et al. 2020

Cancer Cell Int

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“…Subsequent experiments indicated that lncRNA PCAT-1 could enhance DDP resistance of GC cells via regulating the miRNA-128/ZEB1 axis [54]. Another study also demonstrated that knockdown of lncRNA PCAT-1 reversed DDP resistance in GC cells [55]. Mechanically, resistance of GC cells to DDP modulated by lncRNA PCAT-1 was attributed to silenced phosphatase and tensin homolog (PTEN) via interacting with enhancer of zeste homolog 2 (EZH2) [55].…”

Section: Lncrnas and Platinum Resistancementioning

confidence: 99%

The Multifaceted Role of Long Non-Coding RNA in Gastric Cancer: Current Status and Future Perspectives

Li¹,

Lü²,

Wu³

et al. 2021

Int. J. Biol. Sci.

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Gastric cancer (GC) is one of the major public health concerns. Long non-coding RNAs (lncRNAs) have been increasingly demonstrated to possess a strong correlation with GC and play a critical role in GC occurrence, progression, metastasis and drug resistance. Many studies have shed light on the understanding of the underlying mechanisms of lncRNAs in GC. In this review, we summarized the updated research about lncRNAs in GC, focusing on their roles in Helicobacter pylori infection, GC metastasis, tumor microenvironment regulation, drug resistance and associated signaling pathways. LncRNAs may serve as novel biomarkers for diagnosis and prognosis of GC and potential therapeutic targets. The research gaps and future directions were also discussed.

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“…Multiple (Table 8). For instance, lncRNA PCAT-1, a highly expressed lncRNA in DDP-resistant gastric cancer miR-494 ↓ FGFR2 lapatinib [159] tissues and cells, promotes DDP resistance of gastric cancer cells via epigenetically suppressing PTEN expression by recruiting EZH2, as well as regulating the miR-128/ ZEB1 axis [161,162]. Similarly, an evidently high expression lncRNA DANCR has been identified in SGC7901/ DDP and BGC823/DDP DDP-resistant gastric cancer cells.…”

Section: Lncrnas and Resistance To Platinum Drugsmentioning

confidence: 99%

Noncoding RNAs in gastric cancer: implications for drug resistance

et al. 2020

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Gastric cancer is the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide. Advanced gastric cancer patients can notably benefit from chemotherapy including adriamycin, platinum drugs, 5-fluorouracil, vincristine, and paclitaxel as well as targeted therapy drugs. Nevertheless, primary drug resistance or acquisition drug resistance eventually lead to treatment failure and poor outcomes of the gastric cancer patients. The detailed mechanisms involved in gastric cancer drug resistance have been revealed. Interestingly, different noncoding RNAs (ncRNAs), such as microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), are critically involved in gastric cancer development. Multiple lines of evidences demonstrated that ncRNAs play a vital role in gastric cancer resistance to chemotherapy reagents and targeted therapy drugs. In this review, we systematically summarized the emerging role and detailed molecular mechanisms of ncRNAs impact drug resistance of gastric cancer. Additionally, we propose the potential clinical implications of ncRNAs as novel therapeutic targets and prognostic biomarkers for gastric cancer.

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PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2

Cited by 40 publications

References 33 publications

LINC00152 upregulates ZEB1 expression and enhances epithelial-mesenchymal transition and oxaliplatin resistance in esophageal cancer by interacting with EZH2

LINC00152 upregulates ZEB1 expression and enhances epithelial-mesenchymal transition and oxaliplatin resistance in esophageal cancer by interacting with EZH2

The Multifaceted Role of Long Non-Coding RNA in Gastric Cancer: Current Status and Future Perspectives

Noncoding RNAs in gastric cancer: implications for drug resistance

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