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Cancer Biomarkers: Section A of Disease Markers logoLink to Cancer Biomarkers: Section A of Disease Markers
. 2015;15(6):717–723. doi: 10.3233/CBM-150513

MALAT1 might be a predictive marker of poor prognosis in patients who underwent radical resection of middle thoracic esophageal squamous cell carcinoma

Xinguang Cao a,b, Ruihua Zhao c, Qiong Chen b, Yuzhou Zhao b, Bin Zhang b, Yanzhen Zhang b, Juan Yu b, Guangsen Han b, Wei Cao b, Jiansheng Li a,*, Xiaobing Chen b
PMCID: PMC12965489  PMID: 26406400

Abstract

BACKGROUND: Recent studies have demonstrated that MALAT1 is involved in cancer metastasis and recurrence and it is up-regulated in cervical cancer, hepatocellular carcinoma, non-small cell lung cancer (NSCLC) and colorectal cancer. However, the role of MALAT1 in esophageal squamous cell carcinoma (ESCC) is still unclear.

METHODS: The expression of MALAT1 was evaluated in cancer tissue and paired adjacent normal tissue samples from 77 middle thoracic ESCC patients who received radical surgical resection using QRT-PCR. The correlations between the expression levels of MALAT1 and clinical-pathological features and Patients' survival were also analysed.

RESULTS: MALAT1 expression was increased in ESCC tissue than in adjacent normal tissue samples (P< 0.001). MALAT1 level was positively related to pT stage (P= 0.01). Kaplan-Meier analysis showed high expression levels of MALAT1 ware correlated with poor prognosis in ESCC patients. Patients with a high level of MALAT1 had a shorter DFS and OS than those with low MALAT1 expression (P= 0.04 and 0.038, respectively). On Multivariate analysis, The HR of MALAT1 expression was 1.76 (95% CI = 0.97-3.21, P= 0.06) for DFS and 1.81 (95% CI = 0.97-3.41, P$=0.06) for OS.

CONCLUSIONS: Our results showed that MALAT1 expression may serve as a predictive marker for middle thoracic ESCC patients who have been received radical resection.

Keywords: Esophageal squamous cell carcinoma, long non-coding RNA, MALAT1

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Articles from Cancer Biomarkers: Section A of Disease Markers are provided here courtesy of SAGE Publications

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