Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting β-catenin<i>via</i>Ezh2

Wang, Wei; Zhu, Yunan; Li, Sanni; Chen, Xinfeng; Jiang, Guozhong; Shen, Zhibo; Qiao, Ying; Wang, Liping; Zheng, Peng‐Yuan; Zhang, Yi

doi:10.18632/oncotarget.8257

Cited by 89 publications

(75 citation statements)

References 39 publications

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“…Wang et al. recently found that the expression of lncRNA MALAT1 were higher in ESCC tissues and cell lines. Downregulation of MALAT1 decreased the expression of β ‐catenin, Lin28, and EZH2 genes, while overexpressed EZH2 could reverse such suppressive effect, indicating the promotion mechanism of MALAT1 in ESCC.…”

Section: Discussionmentioning

confidence: 98%

AFAP1‐AS1 is upregulated and promotes esophageal squamous cell carcinoma cell proliferation and inhibits cell apoptosis

et al. 2016

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Recent findings indicate that long noncoding RNAs (lncRNAs) were dysregulated in many kinds of tumors including esophageal squamous cell carcinoma (ESCC). LncRNA AFAP1‐AS1 was found to be upregulated in hepatocellular carcinoma (HCC), lung cancer, colorectal cancer, esophageal adenocarcinoma (EAC), pancreatic ductal adenocarcinoma, and nasopharyngeal carcinoma, while its clinical value and potential function in ESCC are still unknown. Expression of AFAP1‐AS1 was measured in 65 ESCC tissues and corresponding noncancerous tissues by quantitative real‐time polymerase chain reaction, which revealed that AFAP1‐AS1 expression was markedly elevated in ESCC tissues and significantly associated with advanced TNM stage (P = 0.004) and larger tumor size (P = 0.040). Moreover, by knocking down AFAP1‐AS1 expression in ESCC cells, the proliferation and colony‐forming ability were inhibited and cell apoptosis was induced. Our data indicated the first time that AFAP1‐AS1, a novel oncogene, was remarkably upregulated and played a critical role in the progression of ESCC.

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Section: Discussionmentioning

confidence: 98%

AFAP1‐AS1 is upregulated and promotes esophageal squamous cell carcinoma cell proliferation and inhibits cell apoptosis

et al. 2016

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“…MALAT1 has been reported to be an oncogenic lncRNA which can promote cancer development by acting as miRNA sponges, regulating autophagy, or accelerating EMT signaling (Chou et al, ; Li et al, ). MALAT1 can promote tumor development in various cancers, such as gallbladder cancer (Wang, Zhu et al, ), gastric cancer (Xia et al, ) and esophageal squamous cell carcinoma (Wang, Yu et al, ). For instance, MALAT1 can promote gallbladder cancer development by sponging miR‐206 (Wang, Zhang, Wu, Weng et al, ).…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

Chang

2017

Journal Cellular Physiology

101

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Oral squamous cell carcinoma (OSCC), as the most common type of oral cancer, is responsible for almost 3% of all malignant tumors worldwide. Non-coding RNAs such as lncRNAs and microRNAs have been involved in many cancers including OSCC. Recently, lncRNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) has been reported to play an oncogenic role in OSCC metastasis. However, the underlying mechanism of MALAT1 in regulating OSCC progression remains unclear. The aim of this study was to investigate the specific role of MALAT1 in OSCC development. It was observed that MALAT1 was upregulated in OSCC cell lines. Inhibition of MALAT1 can prevent OSCC proliferation while overexpressing MALAT1 promoted OSCC progression. In addition, bioinformatics search was used to identify that miR-125b was a direct target of MALAT1, which indicated a negative correlation between MALAT1 and miR-125b. Besides these, STAT3 was predicted as a binding target of miR-125b in OSCC. Overexpression of MALAT1 was able to suppress the tumor inhibitory effect of miR-125b mimics via upregulating STAT3. Moreover, the function of MALAT1 in OSCC development was further investigated by using in vivo assays. The established nude mice models revealed that downregulated MALAT1 greatly inhibited OSCC tumor growth and reversely upregualated MALAT1 promoted OSCC development via miR-125b/STAT3 axis, respectively. In conclusion, MALAT1 can function as a competing endogenous RNA (ceRNA) to modulate STAT3 expression by absorbing miR-125b in OSCC and could be used as a novel therapeutic target in OSCC diagnosis and treatment.

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“…As one of the first identified cancer‐associated lncRNAs, MALAT1 was reported to be overexpressed in gastric cancer (Chen, Liu, Wang et al, 2017), breast cancer (Arun et al, ), prostate cancer (Ren et al, ), cervical cancer (Sun, Qin et al, ), acute myeloid leukemia (Chen, Nagel et al, 2018), medullary thyroid cancer (Chu, Hardin, Schneider, Chen, & Lloyd, ), choriocarcinoma (Shi, Wang, & Yin, ), gallbladder cancer (Sun et al, ), pancreatic cancer (Xie et al, 2017), multiple myeloma (Liu, Wang et al, ), ovarian cancer (Wu et al, 2017), T and natural killer cell lymphoma (Kim, Kim, Yang, Kim, & Yoon, ), acute monocytic leukemia (Huang, Liu et al, ), endometrial stromal sarcoma (Yamada et al, ), myeloma (Cho et al, ), clear cell renal cell carcinoma (Zhang, Yang, Chen, Che, & Zheng, ), esophageal squamous cell carcinoma (Hu et al, ), glioma (Ma, Wang, Li et al, ), osteosarcoma (Cai et al, ), neuroblastoma (Tee et al, ), tongue squamous cell carcinomas (Fang et al, ), hilar cholangiocarcinoma (Tan, Huang, & Li, ), mantle cell lymphoma (Wang, Zhu et al, ), and other tumor tissues. It has been reported that MALAT1 is involved in the regulation of tumor proliferation, apoptosis, invasion, metastasis, and angiogenesis.…”

Section: Physiopathological Role Of Malat1mentioning

confidence: 99%

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

Chen

Huang

et al. 2018

Journal Cellular Physiology

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. MALAT1 is involved in regulating multiple cell behaviors, such as proliferation, apoptosis, differentiation, migration, epithelial-mesenchymal transition, autophagy, and morphological maintenance. Extensive evidence show that MALAT1 plays critical roles in the physiopathological process of embryo implantation, angiogenesis, tissue inflammation, tumor progression, liver fibrosis, cardiovascular remodeling, and diabetes progression by regulating gene transcription, forming RNA-protein complexes with proteins as a structural component, regulating protein activity, assisting protein localization, mediating epigenetic changes, or by acting as a competing endogenous RNA. Furthermore, MALAT1 can affect the sensitivity of chemotherapy and radiotherapy; therefore, it could be used as a potential drug target for chemotherapy and radiotherapy sensitization. The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion. Therefore, MALAT1 can be used as a biomarker for early diagnosis, severity assessment, or prognostic assessment. This review outlines the current understanding of the biological role and function of MALAT1. In the meantime, we have summarized the mechanisms involved in the reulation of MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.

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Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting β-cateninviaEzh2

Cited by 89 publications

References 39 publications

AFAP1‐AS1 is upregulated and promotes esophageal squamous cell carcinoma cell proliferation and inhibits cell apoptosis

AFAP1‐AS1 is upregulated and promotes esophageal squamous cell carcinoma cell proliferation and inhibits cell apoptosis

Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1

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