<p>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</p>

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.

Pathways and role of MALAT1 in esophageal and gastric cancer (Review)

“…Their results indicated that the MALAT1/miR-1297/HMGB2 axis is important for the regulation of GC tumorigenesis and progression, and may serve as a therapeutic target for GC. In a study conducted by Li et al (23), transfected cells with overexpressed or silenced MALAT1 were prepared, and their proliferation and apoptosis, as well as the tumor volume and weight when injected into mice were evaluated. The overexpression of MALAT1 promoted proliferation and inhibited apoptosis via the upregulation of miR-22-3p and downregulation of ErbB3, while the knockdown of MALAT1 inhibited GC tumor growth in mice.…”

“…In patients with GC, it has been observed that MALAT1 is upregulated. In particular, MALAT1 is overexpressed in the serum of patients with gastric adenocarcinoma and GC tissues, as well as in GC cell lines (23,26).…”

Identification of a Novel Prognostic Signature for Gastric Cancer Based on Multiple Level Integration and Global Network Optimization

“…After multiple-level random walk analyses, we further calculated the IRW score for each candidate signature and the signature with a higher score was regarded as GC prognostic signature. MiR-22 was ranked top one in all candidates, and the regulatory roles of miR-22-3p were confirmed by the proliferation and apoptosis of GC cells (Li et al, 2020). MiR-125a (ranked second) restrained cell migration and invasion by targeting STAT3 in GC Cells (Yang et al, 2019).…”

The expression and prognostic value of the epidermal growth factor receptor family in glioma

“…ERBB3 is closely related to the occurrence and development of various tumors. Abnormal activation and overexpression of the HER3 gene can be seen in malignant tumors such as breast cancer [ 60 ], gastric cancer [ 61 ], ovarian cancer [ 62 ], and prostate cancer [ 63 ].…”