Silencing of LncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Inhibits the Proliferation and Promotes the Apoptosis of Gastric Cancer Cells Through Regulating microRNA-22-3p-Mediated ErbB3
Authors: Xiaoning Li
Jianhui Cai
Jiangqiao Zhao
Huiqing Zhang
Journal: OncoTargets and therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNA22-3p; epidermal growth factor receptor 3; gastric cancer; long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1.
Affiliations: Department of Surgery, Hebei Medical University, Shijiazhuang, Hebei 050017, People's Republic of China., Department of General Surgery, Hebei General Hospital, Shijiazhuang, Hebei 050051, People's Republic of China., Department of General SurgeryⅡ, Baoding First Central Hospital, Baoding, Hebei 071000, People's Republic of China., Department of General Surgery, Cangzhou People's Hospital, Cangzhou, Hebei 061000, People's Republic of China., Department of Medical, Baoding First Central Hospital, Baoding, Hebei, People's Republic of China.

Abstract:  Purpose: This study aimed to investigate the regulatory effects and mechanisms of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on gastric cancer (GC) cells. Methods: The expression of MALAT1 was detected in GC tissues and two GC cell lines (SGC-7901 and BGC-823). MALAT1 was overexpressed and silenced in GC cells by the transfection of pcDNA-MALAT1 and siRNA-MALAT1, respectively. The proliferation and apoptosis of transfected cells, as well as the tumor volume and weight in mice injected with transfected cells were determined. After identifying the interaction between microRNA-22-3p (miR-22-3p) and MALAT1/epidermal growth factor receptor 3 (ErbB3), the effects of miR-22-3p/ErbB3 silencing on the proliferation and apoptosis of GC cells were evaluated. Results: MALAT1 was significantly upregulated in GC tissues and cells and negatively associated with the survival of GC patients. Overexpression of MALAT1 significantly promoted the proliferation and inhibited the apoptosis of SGC-7901 cells, while silencing of MALAT1 exerts contrary effects on BGC-823 cells. Silencing of MALAT1 also significantly inhibited the tumor growth in mice. In addition, MALAT1 negatively regulated its target miR-22-3p. Silencing of miR-22-3p reversed the anti-tumor effects of MALAT1 silencing on GC cells. MiR-22-3p negatively regulated its target ErbB3. Silencing of ErbB3 reversed the tumor-promoting effects of miR-22-3p silencing on GC cells. Conclusion: Silencing of MALAT1 inhibited the proliferation and promoted the apoptosis of GC cells through upregulating miR-22-3p and downregulating ErbB3. 

Retracted: No

PubPeer comments:
 https: twitter.com vortuosity status 1371056366304043008 , 
 As far as I can tell, the authors bathe the nerve in pure 10% AgNO3 for about 30 minutes.  The steps for chemical treatment of the nerve were as follows: (1) tissues immersed in a 10% AgNO3 solution in a container for 30 min in a dark box in a dark room  As in IBA, stimulation was applied during step 1. The AgNO3 solution, which would be 0.6M(?), doesn t seem hugely physiological. Could the labelling be related to accelerated tissue death because of the stimulation? Also, if there is no sodium in the external solution, how can sodium current flow when the nerve is stimulated? And if sodium currents can t flow, how can [Node of Ranvier [act] as an Array of Bio-Nanoantennas for Infrared Communication in Nerve Tissue] ?? ,