J Cancer 2020; 11(23):6892-6901. doi:10.7150/jca.48426 This issue

Research Paper

TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

Qing Liu1,2#, Shutao Zheng1,2#, Yumei Chen2, Tao Liu3, Xiujuan Han2, Xiao Zhang2, Tongxue Shen2, Xiaomei Lu1,2✉

1. Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi, PR China.
2. State Key Laboratory of Pathogenesis, Prevention, Treatment of High Incidence Diseases in Central Asian, Xinjiang Uygur Autonomous Region, Urumqi, PR China.
3. Health Management Center, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi, PR China.
#Co-first authors.

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Citation:
Liu Q, Zheng S, Chen Y, Liu T, Han X, Zhang X, Shen T, Lu X. TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT. J Cancer 2020; 11(23):6892-6901. doi:10.7150/jca.48426. Available from https://www.jcancer.org/v11p6892.htm

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Abstract

Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both in vivo and in vitro. Furthermore, knockdown of MALAT1 inhibited TGF-β1-induced EMT. Our data indicate that MALAT1 is heavily involved in EMT induced by TGF-β1. MALAT1 may be a therapeutic target in the suppression of metastasis and invasion of ESCC.

Keywords: Kazakh's ESCC, EMT, TGF-β1, MALAT1