Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion
Authors: A Zou
X Wu
R Liu
Journal: Neoplasma (2016)
Discipline: CLINICAL MEDICINE
Keywords: MALAT1; invasion mitogen-activated protein kinase.; ovarian cancer; proliferation.

Abstract:  Ovarian cancer is a gynecological malignancy worldwide. Long non-coding RNAs (lncRNAs) research is an emerging area in cancer studies, but little is known about lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in ovarian cancer. This study aims to investigate expression and roles of MALAT1 in ovarian cancer. MALAT1 level was detected in 20 ovarian cancer patients. MALAT1 expression was promoted by transforming growth factor Œ≤1 (TGFB1) treatment and inhibited by siRNA transfection in human ovarian cancer cell line SK-OV-3, after which changes in cell viability, proliferation, migration and invasion were analyzed by MTT, colony formation and Transwell assays. Protein levels of mitogen-activated protein kinase factors, including MAPK kinase 1 (MEK1), extracellular signal-regulated kinase (ERK1), p38 and c-Jun N-terminal kinase 1 (JNK1), were detected by western blot. Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P &lt; 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P &lt; 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P &lt; 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1. This study reveals that MALAT1 is a potential biomarker for tumor growth and metastasis, as well as a promising therapeutic target in ovarian cancer, facilitating further ovarian cancer research. 

Retracted: No

PubPeer comments:
 This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: * https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) * https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: * Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 * Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 , 
 Fig 3A C. Two panels appear to have been copied from *[right]* Fig 4B of  Genome-Wide Screening Identified That miR-134 Acts as a Metastasis Suppressor by Targeting Integrin u03b21 in Hepatocellular Carcinoma ([Zha et al 2014] ).  Other panels are details of panels from Fig 4B C,  SOX2 enhances the migration and invasion of ovarian cancer cells via Src kinase} ([Wang et al 2014] ).  ,