STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy

The mechanism underlying the poor prognosis of gastric cancer, including its high degree of malignancy, invasion, and metastasis, is extremely complicated. Rho GTPases are involved in the occurrence and development of a variety of malignant tumors. ARHGAP11A, in the Rho GTPase activating protein family, is highly expressed in gastric cancer, but its function and mechanism have not yet been explored. In this study, the effect of ARHGAP11A on the occurrence and development of gastric cancer and the mechanism related to this effect were studied. The expression of ARHGAP11A was increased in gastric cancer cells and tissues, and high ARHGAP11A expression in tissues was related to the degree of tumor differentiation and poor prognosis. Moreover, ARHGAP11A knockout significantly inhibited cell proliferation, cell migration, and invasion in vitro and significantly inhibited the tumorigenic ability of gastric cancer cells in nude mice in vivo. Further studies revealed that ARHGAP11A promotes the malignant progression of gastric cancer cells by interacting with TPM1 to affect cell migration and invasion and the stability of actin filaments. These results suggest that ARHGAP11A plays an important role in gastric cancer and may become a useful prognostic biomarker and therapeutic target for gastric cancer patients.

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Inhibiting PP2Acα Promotes the Malignant Phenotype of Gastric Cancer Cells through the ATM/METTL3 Axis

BioMed Research International ◽

10.1155/2021/1015293 ◽

2021 ◽

Vol 2021 ◽

pp. 1-16

Author(s):

Zhaoxiang Cheng ◽

Shan Gao ◽

Xiaojie Liang ◽

Chao Lian ◽

Jianquan Chen ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Catalytic Subunit ◽

Malignant Progression ◽

Malignant Phenotype ◽

Gastric Cancer Cells ◽

Internal Connection ◽

Phosphatase 2A ◽

The Relationship

This article is aimed at exploring the relationship between the phosphatase 2A catalytic subunit Cα (PP2Acα, encoded by PPP2CA) and methyltransferase-like 3 (METTL3) in the malignant progression of gastric cancer (GC). Through analyzing the bioinformatics database and clinical tissue immunohistochemistry results, we found that abnormal PP2Acα and METTL3 levels were closely related to the malignant progression of GC. To explore the internal connection between PP2Acα and METTL3 in the progression of GC, we carried out cellular and molecular experiments and finally proved that PP2Acα inhibition can upregulate METTL3 levels by activating ATM activity, thereby promoting the malignant progression of GC.

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circABCB10 Promotes Malignant Progression of Gastric Cancer Cells by Preventing the Degradation of MYC

Journal of Oncology ◽

10.1155/2021/4625033 ◽

2021 ◽

Vol 2021 ◽

pp. 1-14

Author(s):

Yingchun Zhang ◽

Yong Zhou ◽

Fang Wei

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Malignant Progression ◽

Luciferase Reporter ◽

Regulatory Effect ◽

Gastric Cancer Cells ◽

Subcutaneous Tumor ◽

Tumor Bearing ◽

Gene Assay ◽

Cancer Tissues

Objective. To investigate the role of circABCB10 in gastric cancer and the molecular mechanism of promoting malignant progression of gastric cancer cells by preventing the degradation of MYC by hsa-miR-1252-5p. Methods. The expression of circABCB10 in gastric cancer tissues and cells was detected by real-time quantitative PCR. MTT, Transwell, clone formation, and TUNEL assay were used to detect the effects of circABCB10 on the proliferation, invasion, and apoptosis of gastric cancer cells. A subcutaneous tumor-bearing model was established to study the inhibitory effect of knockdown circABCB10 on gastric cancer proliferation. The dual luciferase reporter gene assay and RNA pull-down assay were used to verify the regulatory effect of circABCB10 on miR-1252-5p and the regulatory effect of miR-1252-5p on MYC. Results. Compared with paracancerous tissues and gastric mucosal epithelial cells, the expression of circABCB10 was significantly increased in human gastric cancer tissues and gastric cancer cells. circABCB10 knockout significantly decreased cell viability and invasion ability and promoted cell apoptosis ( P < 0.01 ). Subcutaneous tumor-bearing experiments in nude mice demonstrated that circABCB10 knockdown inhibited the proliferation of gastric cancer cells. circABCB10 can act as a sponge for miR-1252-5p in gastric cancer cells. Meanwhile, MYC is the target gene of miR-1252-5p. Overexpression of miR-1252-5p and knockdown of MYC reversed the promoting effect of circABCB10 on gastric cancer. Conclusion. circABCB10 can promote the proliferation, invasion, and clonal formation of gastric cancer cells by targeting miR-1252-5p and upregulating the expression of MYC. circABCB10/miR-1252-5p/MYC constitutes the regulatory mechanism of ceRNA.

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