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Tumor suppressor role of hsa_circ_0035445 in gastric cancer.

ABSTRACT: Circular RNAs (circRNAs) are closely related to the occurrence and development of cancers. However, the roles of circRNAs in gastric cancer are largely unknown. Total 104 pairs of gastric cancer tissues and non-cancer tissues, fasting plasma of 42 healthy people and 42 gastric cancer patients' one day before operation and 10 days after operation were collected. Quantitative reverse transcription-polymerase chain reaction was used to detect the expression level of hsa_circ_0035445. The receiver operating characteristic (ROC) curve and the area under the ROC curve (AUC) were used to analyze its diagnostic value. Small interfering RNA and overexpression vector were used to downregulate and upregulate the expression of hsa_circ_0035445, respectively. Cell Counting Kit-8 and colony formation assays were used to detect the proliferation ability. Trans-well assay and scratch assay were used to detect the migration ability. Finally, flow cytometry was used to detect the changes of cell cycle distribution and apoptosis. Hsa_circ_0035445 was lowly expressed in gastric cancer tissues, plasma of gastric cancer patients, and gastric cancer cells. The expression level of hsa_circ_0035445 in gastric cancer tissues was relationship with tumor size and distant metastasis. The AUC of hsa_circ_0035445 in tissues and plasma was 0.68 and 0.86, respectively. Upregulation of hsa_circ_0035445 suppressed the proliferation and migration, promoted apoptosis, and blocked cells at G0/G1 phase. Downregulation of hsa_circ_0035445 promoted the proliferation and migration, suppressed apoptosis, and blocked cells at S phase. In conclusion, hsa_circ_0035445 may become a new target for the treatment of gastric cancer.

SUBMITTER: Sun W

PROVIDER: S-EPMC8183929 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Gastric cancer is the second leading cause of cancer death and remains a major clinical challenge due to poor prognosis and limited treatment options. Therefore, the basic mechanisms underlying gastric tumorigenesis deserve investigation. Although regulation of the galactoside-binding lectin galectin-7 in cancer has been studied, its role in tumor formation and progression remains controversial. In this study, we investigated galectin-7 expression and its role in gastric cancer. Immunohistochemical staining using a tissue microarray of gastric cancer patients revealed significantly low expression levels of galectin-7 in malignant tissues compared with matched normal tissues, and decreased expression of galectin-7 in malignant tissues was associated with advanced TMN stage disease (p=0.034). Importantly, low expression of galectin-7 in normal tissues was associated with a poor survival rate (p=0.0561). Over-expression of galectin-7 in AGS gastric adenocarcinoma cells suppressed cell proliferation, migration, and invasion, whereas ablation of galectin-7 in KATO III gastric carcinoma cells reversed these properties. AGS cells that overexpressed galectin-7 could not form gastric tumors in xenografted mice. More than 70% hypermethylation was observed in 7 of 9 gastric cancer cell lines tested and 5-aza-cytidine treatment lowered galectin-7 expression by reducing methylation in 24 cancer cell lines from five different organ origins. We analyzed CpG islands in the galectin-7 genomic region and detected hypermethylation at +1566bp of exon 2, the predicted p53 binding region. DNA hypermethylation of this region was also detected in gastric cancer tissues from 20 patients. Taken together, our data indicate that galectin-7 has a tumor suppressive function, and that the gene is epigenetically modified by DNA methylation and significantly down-regulated in gastric cancer. Further study of galectin-7 regulation may lead to improved gastric cancer diagnosis and therapy.

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Tumor suppressor role of hsa_circ_0035445 in gastric cancer.

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