Long noncoding RNA LSINCT5 promotes endometrial carcinoma cell proliferation, cycle, and invasion by promoting the Wnt/β-catenin signaling pathway HMGA2.

Ther Adv Med Oncol

Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan Two Road, Yuexiu District, Guangzhou, Guangdong 510080, China.

Published: September 2019

Background: A review of the evidence has indicated the critical role of long noncoding RNA (lncRNA) LSINCT5 in a large number of human cancers. However, the mechanistic involvement of LSINCT5 in endometrial carcinoma (EC) is still unknown. Here the authors aim to characterize the expression status of LSINCT5 and elucidate its mechanistic relevance to EC.

Methods: Relative expression of LSINCT5 and HMGA2 were quantified by a real-time polymerase chain reaction. SiRNAs were employed to specifically knockdown endogenous LSINCT5 in EC cells. Cell proliferation was measured with Cell Count Kit-8 kit (CCK-8, Dojindo, Kumamoto, Japan) and cell growth was assessed by a colony formation assay. The cell cycle was analyzed with propidium iodide (PI) staining. Apoptotic cells were determined by flow cytometry after Annexin V/PI double-staining. Cell migration was evaluated by a wound-healing assay, and cell invasion was assessed using a transwell migration assay. The protein levels of HMGA2, Wnt3a, p-β-catenin, c-myc, β-actin, and GAPDH were determined by western blot.

Results: The authors observed positively correlated and aberrantly up-regulated LSINCT5 and HMGA2 in EC. LSINCT5 deficiency significantly inhibited cell proliferation, cell cycle progression, and induced apoptosis. Meanwhile, cell migration and invasion were greatly compromised by the LSINCT5 knockdown. LSINCT5 stabilized HMGA2, which subsequently stimulated activation of Wnt/β-catenin signaling and consequently contributed to the oncogenic properties of LSINCT5 in EC.

Conclusions: Our data uncovered the oncogenic activities and highlighted the mechanistic contributions of the LSINCT5-HMGA2-Wnt/β-catenin signaling pathway in EC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769207PMC
http://dx.doi.org/10.1177/1758835919874649DOI Listing

Publication Analysis

Top Keywords

cell proliferation
12
lsinct5
11
cell
10
long noncoding
8
noncoding rna
8
endometrial carcinoma
8
wnt/β-catenin signaling
8
signaling pathway
8
lsinct5 hmga2
8
assay cell
8

Similar Publications

Exosomal circ_0006896 promotes AML progression via interaction with HDAC1 and restriction of antitumor immunity.

Mol Cancer

January 2025

Department of Hematology, Qilu Hospital of Shandong University, No.117, West of Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.

Background: Drug resistance and immune escape continue to contribute to poor prognosis in AML. Increasing evidence suggests that exosomes play a crucial role in AML immune microenvironment.

Methods: Sanger sequencing, RNase R and fluorescence in situ hybridization were performed to confirm the existence of circ_0006896.

View Article and Find Full Text PDF

Tribbles homolog 2 (TRIB2), a pseudoserine/threonine kinase, is a member of the TRIB family. TRIB2 primarily regulates cell proliferation through its scaffold or adaptor effect on promoting the degradation of target proteins by E3 ligase-dependent ubiquitination and regulating mitogen-activated protein kinase (MAPK) and protein kinase B (AKT) signaling pathways. TRIB2 is not only involved in the physiological proliferation of cells (granulosa cells, myoblasts, naive T cells, and thymocytes) during normal development but also in the pathological proliferation of vascular smooth muscle cells and a variety of cancer cells (lung cancer cells, liver cancer cells, leukemia cells, pancreatic cancer cells, gastric cancer cells, prostate cancer cells, thyroid cancer cells, cervical cancer cells, melanoma cells, colorectal cancer cells, ovarian cancer cells and osteosarcoma cells) under disease conditions.

View Article and Find Full Text PDF

Background: Gastric cancer (GC) is known for its high heterogeneity, presenting challenges in current clinical treatment strategies. Accurate subtyping and in-depth analysis of the molecular heterogeneity of GC at the molecular level are still not fully understood.

Methods: This study categorized GC into two subtypes based on apoptosis-related genes (ARGs) and investigated differences in tumor immune microenvironment, intratumoral microorganisms distribution, gene expression, and signaling pathways.

View Article and Find Full Text PDF

P-cadherin (pCAD) and LI-cadherin (CDH17) are cell-surface proteins belonging to the cadherin superfamily that are both highly expressed in colorectal cancer. This co-expression profile presents a novel and attractive opportunity for a dual targeting approach using an antibody-drug conjugate (ADC). In this study, we used a unique avidity-driven screening approach to generate pCAD x CDH17 bispecific antibodies that selectively target cells expressing both antigens over cells expressing only pCAD or only CDH17.

View Article and Find Full Text PDF

We studied the effect of acteoside on a model of human corneal epithelial cells (HCEC) injury induced by HO. HCEC were divided into 4 groups and cultured for 24 h in normal medium (intact and control groups, respectively), or in a medium containing DMSO or 160 μM acteoside (DMSO and acteoside groups, respectively). Then, HO solution was added to HCEC for 4 h, except for intact cells.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!