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Glyoxalase 1, regulated by LncRNA MALAT1, promotes malignant development of esophageal squamous cell carcinoma.

ABSTRACT: In previous study we found that long noncoding RNA (lncRNA) MALAT1 promotes proliferation and metastasis of esophageal squamous cell carcinoma (ESCC), and that the following microarray chip screening of MALAT1 target genes showed that Glyoxalase I (GLO1) was a potential downstream effector of MALAT1. In this study, we further confirmed that GLO1 was regulated by MALAT1. GLO1 belongs to the glyoxalase system, which encodes a ubiquitous detoxification pathway being implicated in the progression of multiple malignancies. However, currently, the role of GLO1 in human ESCC remains unclear. To explore the clinical significance of GLO1 in ESCC, we first determined the expression of GLO1 in 40 paired ESCC tissues and adjacent normal tissues. We found that the expression level of GLO1 was higher in human ESCC tissues (P=0.0040). Knockdown of GLO1 by siRNA significantly inhibited the proliferation and migration of ESCC cells. In vivo assays showed that knockdown of GLO1 decreased tumor growth. Overall, GLO1 might be an essential effector of lncRNA MALAT1 which promotes ESCC progression and can be identified as a potential therapeutic target for ESCC in the future.

SUBMITTER: Guo Z

PROVIDER: S-EPMC6958265 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Glyoxalase 1, regulated by LncRNA MALAT1, promotes malignant development of esophageal squamous cell carcinoma.

Guo Zhong Z Hu Liwen L Luo Jing J Xu Yang Y Diao Yifei Y Ji Saiguang S Cong Zhuangzhuang Z Shen Yi Y

International journal of clinical and experimental pathology 20180501 5

In previous study we found that long noncoding RNA (lncRNA) MALAT1 promotes proliferation and metastasis of esophageal squamous cell carcinoma (ESCC), and that the following microarray chip screening of MALAT1 target genes showed that Glyoxalase I (GLO1) was a potential downstream effector of MALAT1. In this study, we further confirmed that GLO1 was regulated by MALAT1. GLO1 belongs to the glyoxalase system, which encodes a ubiquitous detoxification pathway being implicated in the progression of ...[more]

PMID: 31938345

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Project description:The aim of the present study was to examine the function of transgelin (TAGLN) and its underlying mechanism in the ferroptosis of esophageal squamous cell carcinoma (ESCC) cells. To meet this aim, the association between TAGLN expression and the prognosis of patients with ESCC was determined using tissue samples and clinical data. Gene Expression Omnibus databank and Gene Set Enrichment Analysis data were used to examine which genes were co‑expressed with TAGLN, as well as the influence of TAGLN on ESCC. Subsequently, Transwell chamber, wound healing, Cell Counting Kit‑8 viability and colony formation assays were performed to observe the effects of TAGLN on the migration, invasion, viability and proliferation of Eca‑109 and KYSE‑150 cells. The interaction between TAGLN and p53 in the regulation of ferroptosis was detected using reverse transcription‑quantitative PCR, co‑immunoprecipitation and fluorescence co‑localization assays, and a xenograft tumor model was established to examine the effect of TAGLN on tumor growth. The level of TAGLN expression in patients with ESCC was found to be low, compared with normal esophageal tissue, and a positive association was identified between the prognosis of ESCC and TAGLN expression. The expression of the ferroptosis marker protein, glutathione peroxidase 4, was found to be high, whereas that of acyl‑CoA synthetase long‑chain family member 4 was lower in patients with ESCC compared with expression levels in healthy patients. The overexpression of TAGLN resulted in a significant decrease in the invasive and proliferative capabilities of Eca‑109 and KYSE‑150 cells in vitro compared with the control group; in vivo, TAGLN overexpression was found to significantly decrease tumor size, volume and weight after one month of growth. In addition, the proliferation, migration and invasion of Eca‑109 cells in vivo was stimulated by the knockdown of TAGLN. The results of the transcriptome analysis further demonstrated that TAGLN was able to induce ferroptosis‑associated cell functions and pathways. Finally, TAGLN overexpression was found to promote ferroptosis in ESCC through its interaction with p53. Taken together, the findings of the present study suggested that the malignant development of ESCC may be inhibited by TAGLN through the manifestation of ferroptosis.

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Glyoxalase 1, regulated by LncRNA MALAT1, promotes malignant development of esophageal squamous cell carcinoma.

Publications

Glyoxalase 1, regulated by LncRNA MALAT1, promotes malignant development of esophageal squamous cell carcinoma.

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