Long non-coding RNA MALAT1 is upregulated and involved in cell proliferation, migration and apoptosis in ovarian cancer

Abstract

Abstract. Ovarian cancer (OC) is the leading cause of mortality among gynecological malignancies. Although microRNAs are known to have a key regulatory role in OC, the involvement of long non-coding RNAs in the disease is less established. Previous studies have demonstrated that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a tumor oncogene in many cancers, though its role in OC remains unclear. The present study reported that MALAT1 expression was markedly upregulated in OC, by knockdown of MALAT1 expression in vivo, using RNA interference (RNAi) with small-interfering RNA (siRNA). It was found that MALAT1 expression was positively correlated with the International Federation of Gynecology and Obstetrics stages of OC, tumor histological grade and lymph node metastasis. In addition, the differential MALAT1 levels between a human ovarian epithelial cell line (HOSE) and OC cell lines (ES-2, OVCAR3, SKOV3 and HO8910) were compared in vitro. Notably, MALAT1 was expressed to a high level in OC cells. Furthermore, exogenous knockdown of MALAT1 significantly repressed growth and migration of OC cells, and promoted their apoptosis. Collectively, the current findings suggest that upregulation of MALAT1 in OC may facilitate tumorigenesis and metastasis. Knockdown of MALAT1 expression has potential as a novel target for the diagnosis and therapy of OC.

The HMGB1-2 Ovarian Cancer Interactome. The Role of HMGB Proteins and Their Interacting Partners MIEN1 and NOP53 in Ovary Cancer and Drug-Response

“…As above reported, MALAT1, a lncRNA, previously related to ovarian cancer [ 22 , 23 , 24 , 25 , 26 , 27 ], and to epithelial to mesenchymal transition (EMT) [ 28 ], was detected in our results of EOC-HMGB1-interactome ( Table 1 ). We verified by sequencing that the micropeptide derived from MALAT1 lncRNA, MTEVEMKLLHGVKNVFKRKLRERTTEPRINTNRRAMLLD, is in frame and fused to GAL4 in the recovered Y2H clone.…”

Exosome-mediated delivery of MALAT1 induces cell proliferation in breast cancer

“…MALAT1 expression levels are dysregulated in a variety of cancers, including HCC, 31 , 32 renal cell carcinoma, 33 cholangiocarcinoma, 34 pancreatic cancer, 35 , 36 lung cancer, 37 , 38 gastric cancer, 39 , 40 oral squamous cell carcinoma 41 and ovarian cancer. 42 – 44 In our previous study, we found that MALAT1 was upregulated in breast cancer tissues and cancer cell lines, 45 but MALAT1 interaction with other tumor cells in the tumor microenvironment still needs further study. In the present study, we revealed tumor cells secreted MALAT1 to recipient cells to regulate receptor cell proliferation in tumor microenvironment.…”

miR‐211 sponges lncRNA MALAT1 to suppress tumor growth and progression through inhibiting PHF19 in ovarian carcinoma

“…Jin et al (34) have reported that MALAT1 promotes epithelial OC cell proliferation and metastasis via modulation of the PI3K-AKT pathway. Wu et al (35) have also shown that MALAT1 is elevated in OC and is involved in cell proliferation, apoptosis, and migration. However, the molecular mechanisms underlying MALAT1 in OC progression, especially the interaction between MALAT1 and miRNA, are not fully understood.…”