Oct-4 is associated with gastric cancer progression and prognosis

Jiang, Wenli; Zhang, Pengfei; Li, Guofeng; Dong, Jianhua; Wang, Xuesong; Wang, Yuan-Yu

doi:10.2147/ott.s90031

Cited by 10 publications

(3 citation statements)

References 20 publications

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“…The gene contains five exons with a length of 16.40 kB, and it has five transcription start points that can be used to transcribe different mRNAs, which are translated into a variety of proteins. During embryonic development, the expression level of Oct4 affects the differentiation and dedifferentiation of embryonic stem cells, maintaining the self-renewal ability of the embryonic stem cells 22. In terms of tumors, Oct4 is usually highly expressed in germ and embryonic tumor cells, such as germ tumor cells, asexual tumor cell seminoma, and embryonal carcinoma 23.…”

Section: Discussionmentioning

confidence: 99%

Effect of overexpression of Oct4 and Sox2 genes on the biological and oncological characteristics of gastric cancer cells

Chen

Zhu

et al. 2019

OTT

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Objective: Using the gastric cancer cell line SGC7901, we constructed a cell line that overexpressed octamer-binding protein 4 (Oct4) and SRY-box 2 (Sox2) to explore the stem cell oncological and biological characteristics of these cells and to elucidate the mechanisms of Oct4 and Sox2 in cancer. Methods: A lentiviral vector containing the Sox2 gene was constructed and transfected into a gastric cancer cell line overexpressing Oct4 (SGC7901-Oct4) to obtain a stably transfected cell line (SGC7901-Oct4-Sox2). Oct4 and Sox2 expression was detected by RT-PCR and Western blotting. The proliferation, drug resistance, migration, and invasion abilities of the cells were assessed using in vitro (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium), drug resistance, scratch-wound migration, transwell migration, transwell invasion, and spherical clone formation assays, and their tumorigenic ability was assessed using a tumor formation experiment in mice. Results: Compared with the control group, the expression of Oct4, Sox2, CD44, and E-cadherin was significantly higher in the group that overexpressed Oct4 and Sox2, while the expression of c-Myc and Klf4 did not significantly change. The proliferation, drug resistance, migration, and invasion abilities were significantly enhanced in the overexpression group, and the tumorigenic ability in mice was also significantly enhanced, with significantly increased tumor size and weight. Conclusion: The proliferation, drug resistance, migration, invasion, and tumorigenic abilities of SGC7901 cells overexpressing Oct4 and Sox2 were significantly improved. Oct4 and Sox2 play important roles in the proliferation, migration, invasion, and tumorigenicity of gastric cancer cells, and the two genes may be synergistic to a certain degree.

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Section: Discussionmentioning

confidence: 99%

Effect of overexpression of Oct4 and Sox2 genes on the biological and oncological characteristics of gastric cancer cells

Chen

Zhu

et al. 2019

OTT

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“…Gastric cancer (GC) is one among the foremost common malignant neoplasms within the digestive tract and is the fourth common malignancy and the third leading cause of cancer-related death worldwide (1,2). GC patients tend to be diagnosed at advanced stages, and the 5-year survival rate is no more than 40% in China (3). Although Helicobacter pylori has been reported as the most significant risk factor for GC (4), the exact etiology of GC is still unclear, and a detailed investigation of molecular mechanisms of GC is urgently needed to identify novel therapeutic and diagnostic targets.…”

Section: Introductionmentioning

confidence: 99%

DEK modulates both expression and alternative splicing of cancer‑related genes

et al. 2022

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DEK is known to be a potential proto-oncogene and is highly expressed in gastric cancer (GC); thus, DEK is considered to contribute to the malignant progression of GC. DEK is an RNA-binding protein involved in transcription, DNA repair, and selection of splicing sites during mRNA processing; however, its precise function remains elusive due to the lack of clarification of the overall profiles of gene transcription and post-transcriptional splicing that are regulated by DEK. We performed our original whole-genomic RNA-Seq data to analyze the global transcription and alternative splicing profiles in a human GC cell line by comparing DEK siRNA-treated and control conditions, dissecting both differential gene expression and potential alternative splicing events regulated by DEK. The siRNA-mediated knockdown of DEK in a GC cell line led to significant changes in gene expression of multiple cancer-related genes including both oncogenes and tumor suppressors. Moreover, it was revealed that DEK regulated a number of alternative splicing in genes which were significantly enriched in various cancer-related pathways including apoptosis and cell cycle processes. This study clarified for the first time that DEK has a regulatory effect on the alternative splicing, as well as on the expression, of numerous cancer-related genes, which is consistent with the role of DEK as a possible oncogene. Our results further expand the importance and feasibility of DEK as a clinical therapeutic target for human malignancies including GC.

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“…1,2 Patients are diagnosed at the advanced stages of gastric cancer and 5-year survival rate is no more than 40% in China. [3][4][5] Surgical resection, radiation therapy, chemotherapy and combination treatments are considered as therapeutic approaches for malignancies, including gastric cancer. 4 Despite this, more than 80% of the cancer patients develop loco-regional or distant recurrence after curative resection.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway

Jian¹,

Sun³

et al. 2019

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Objectives: Gastric cancer ranks the fourth most common cancer and the third leading cause of cancer mortality in the world. ROS proto-oncogene 1 (ROS1) is an oncogene and ROS1 rearrangement has been reported in many cancers. Our study aimed to investigate the potential function and the precise mechanisms of ROS1 in gastric cancer. Methods: In our study, the analysis of ROS1 expression and clinical pathologic factors of gastric cancer in gastric cancer using TCGA database demonstrated that ROS1 expression was elevated in gastric cancer and related to T, N, M and TNM staging. High expression of ROS1 predicted poor survival in patients with gastric cancer. Then, we measured ROS1 expression in four human gastric cancer cell lines and knocked down ROS1 expression in BGC-823 and SGC-7901 cells by specific shRNA transfection via Lipofectamine 2000. The effect of ROS1 knockdown on cell proliferation, cell cycle distribution, cell apoptosis and metastasis in vitro was evaluated by MTT, colony formation, flow cytometric analysis, wound healing and Transwell invasion assays. The levels of apoptosis-related proteins, EMT markers and the PI3K/Akt signaling pathway members were measured by Western blotting. Results: We demonstrated that shROS1 transfection markedly downregulated ROS1 expression in BGC-823 and SGC-7901 cells. Knockdown of ROS1 inhibited cell survival, clonogenic growth, migration, invasion and epithelial-mesenchymal transition (EMT), as well as induced cell cycle arrest and apoptosis in gastric cancer cells. Furthermore, ROS1 knockdown inhibited the phosphorylation of PI3K and Akt. Conclusion: Collectively, our data suggest that ROS1 may serve as a promising therapeutic target in gastric cancer treatment.

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Oct-4 is associated with gastric cancer progression and prognosis

Cited by 10 publications

References 20 publications

<p>Effect of overexpression of Oct4 and Sox2 genes on the biological and oncological characteristics of gastric cancer cells</p>

<p>Effect of overexpression of Oct4 and Sox2 genes on the biological and oncological characteristics of gastric cancer cells</p>

DEK modulates both expression and alternative splicing of cancer‑related genes

<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

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