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LncRNA PTCSC3 and lncRNA HULC Negatively Affect Each Other to Regulate Cancer Cell Invasion and Migration in Gastric Cancer.

ABSTRACT: Background:LncRNA PTCSC3 (PTCSC3) inhibits thyroid cancer cervical carcinoma and glioma, while its roles in gastric cancer are unknown. Studies have reported that HULC could serve as a potential biomarker for the diagnosis and prognosis of gastric cancer (GC). Our study aimed to investigate the potential interaction between PTCSC3 and HULC in gastric cancer. Methods:This study enrolled 77 gastric cancer patients at the First Affiliated Hospital of Anhui Medical University from January 2016 to January 2018. RT-qPCR was performed to analyze gene expression levels. Cell transfections were carried out to evaluate gene interactions. Transwell assays and wound healing assays were used to analyze the effects of transfection on cell invasion and migration. Western blotting was also used to illustrate the possibility that lncRNA PTCSC3 and lncRNA HULC negatively affected each other through WNT signal path. Results:We showed that PTCSC3 was downregulated in tumor tissues of gastric cancer patients in comparison to that in adjacent healthy tissues, and an inverse correlation between the expression levels of PTCSC3 and AJCC stage was observed. LncRNA HULC (HULC) was upregulated in tumor and inversely correlated with PTCSC3 in tumor tissues. Overexpression of PTCSC3 mediated the inhibition of HULC, while overexpression of HULC also mediated the inhibition of PTCSC3. PTCSC3 inhibited, while HULC promoted invasion and migration of gastric cancer cells. In addition, overexpression of HULC attenuated the effects of overexpression of PTCSC3. However, overexpression of PTCSC3 showed no significant effects on cell proliferation. We also found that PTCSC3/HULC affected each other to regulate cell invasion and migration through the Wnt/?-catenin signaling. Conclusion:Therefore, overexpression of PTCSC3 inhibited the invasion and migration of gastric cancer cells, and the function of PTCSC3 is associated with HULC.

SUBMITTER: Cai Y

PROVIDER: S-EPMC7502400 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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LncRNA PTCSC3 and lncRNA HULC Negatively Affect Each Other to Regulate Cancer Cell Invasion and Migration in Gastric Cancer.

Cai Yi Y Li Yang Y Sun Bin B Wang Hugen H Zhang Weiping W Zhao Yuanyuan Y Zhao Haodong H Zhang Jianlin J Xu Jianming J Wang Yalei Y

Cancer management and research 20200916

<h4>Background</h4>LncRNA PTCSC3 (PTCSC3) inhibits thyroid cancer cervical carcinoma and glioma, while its roles in gastric cancer are unknown. Studies have reported that HULC could serve as a potential biomarker for the diagnosis and prognosis of gastric cancer (GC). Our study aimed to investigate the potential interaction between PTCSC3 and HULC in gastric cancer.<h4>Methods</h4>This study enrolled 77 gastric cancer patients at the First Affiliated Hospital of Anhui Medical University from Jan ...[more]

PMID: 32982446

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Project description:BackgroundLong non-coding RNAs (lncRNAs) play critical roles in gastric cancer (GC) initiation progression. However, the biological function of the lncRNA telomerase RNA component (TERC) remains unknown in human GC. The present study sought to determine the biological function and underlying molecular mechanism of the lncRNA TERC in GC progression.MethodsThe expression levels of the lncRNA TERC in GC tissues and cell lines were analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The effects of the lncRNA TERC on the proliferation, migration, and invasion of GC cells were determined using Cell Counting Kit-8 (CCK-8) and Transwell assays. Dual luciferase reporter and argonaute 2 (AGO2)-RNA immunoprecipitation (RIP) assays were used to detect the binding between the lncRNA TERC and microRNA-423-5p (miR-423-5p). Western blotting was performed to measure the expression levels of sex determining region Y-box 12 (SOX12), N-cadherin, E-cadherin, matrix metallopeptidase 9 (MMP9), and proliferating cell nuclear antigen (PCNA).ResultsThe results demonstrated that the lncRNA TERC expression levels were upregulated in GC cells and tissues, while miR-423-5p expression levels were downregulated. The upregulation of the lncRNA TERC was associated with a shorter overall survival in patients with GC. The knockdown of the lncRNA TERC significantly reduced the proliferation, migration, and invasion of human GC cell lines HGC-27 and SNU-1 cells. Further, the lncRNA TERC knockdown in the HGC-27 and SNU-1 cells significantly downregulated the expression levels of SOX12, N-cadherin, MMP9, and PCNA, and upregulated the expression levels of miR-423-5p and E-cadherin. MiR-423-5p was also identified as a target of the lncRNA TERC and was found to directly bind to the lncRNA TERC. Additionally, miR-423-5p was found to directly target SOX12 to inhibit the proliferation, migration, and invasion of the HGC-27 and SNU-1 cells.ConclusionsIn conclusion, the findings of this study suggested that the lncRNA TERC may regulate the miR-423-5p/SOX12 signaling axis by directly sponging miR-423-5p and inhibiting SOX12 expression, thereby leading to the progression of GC. These findings may reveal novel targets for future GC therapy.

Project description:BackgroundPatients with gastric cancer commonly have a poor prognosis, owing to its invasiveness and distant metastasis. Recent studies have confirmed the pivotal role of long non-coding RNAs (lncRNAs) in tumorigenesis and the progression of malignant tumors, including gastric cancer. However, little is known about the molecular mechanism by which lncRNA AK023391 contributes to gastric cancer.MethodsA lncRNA microarray was used to identify the differentially expressed lncRNA AK023391 in gastric cancer and adjacent normal tissues. In addition, RNA fluorescence in situ hybridization (FISH) was used to investigate the association between AK023391 expression and the clinicopathological characteristics and prognosis of patients with gastric cancer. Subsequently, a series of in vitro assays and a xenograft tumor model were used to observe the functions of lncRNA AK023391 in gastric cancer cells. A cancer pathway microarray, bioinformatic analysis, western blotting, and immunochemistry were carried out to verify the regulation of AK023391 and its downstream PI3K/Akt signaling pathway.ResultsExpression of lncRNA AK023391 was significantly upregulated in gastric cancer samples and cell lines in comparison to adjacent normal tissues, and was positively correlated with poor survival in patients with gastric cancer. The multivariate Cox regression model revealed that AK023391 expression acted as an independent prognostic factor for survival in patients with gastric cancer. Knockdown of AK023391 inhibited cell growth and invasion both in vitro and in vivo, and induced apoptosis and cell cycle arrest in gastric cancer cells, whereas its overexpression reversed these effects. Mechanistically, PI3K/Akt signaling mediated the NF-κB, FOXO3a, and p53 pathways. Moreover, downstream transcription factors, such as c-myb, cyclinB1/G2, and BCL-6 might be involved in AK023391-induced tumorigenesis in gastric cancer.ConclusionsThe novel oncogenic lncRNA AK023391 in gastric cancer exerts its effects through activation of the PI3K/Akt signaling pathway, and may act as a potential biomarker for survival in patients with gastric cancer.

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LncRNA PTCSC3 and lncRNA HULC Negatively Affect Each Other to Regulate Cancer Cell Invasion and Migration in Gastric Cancer.

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LncRNA PTCSC3 and lncRNA HULC Negatively Affect Each Other to Regulate Cancer Cell Invasion and Migration in Gastric Cancer.

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