Overexpression of SYF2 promotes cell proliferation and correlates with poor prognosis in human breast cancer

Shi, Feng; Cai, Fengfeng; Cai, Lei; Lin, Xinhua; Zhang, Wei; Wang, Qinqin; Zhao, Yujie; Ni, Qing; Wang, Hua; He, Zhiqiang

doi:10.18632/oncotarget.18188

Cited by 13 publications

(9 citation statements)

References 26 publications

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“…16 Overexpression of SYF2 was also shown could promote breast cancer cell proliferation, while the knockdown of SYF2 led to the cell cycle arrest at G1/S phase. 17 Moreover, SYF2 was reported as indicator for the poor overall survival of patients with esophageal squamous cell carcinoma, breast cancer, or hepatocellular carcinoma. [15][16][17] In this report, luciferase activity reporter assay showed miR-376c-3p could directly binding with the 3 0 -UTR of SYF2.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Influence of miR-376c-3p/SYF2 Axis on the Progression of Gastric Cancer

Liu

Zhang

et al. 2019

Technol Cancer Res Treat

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MicroRNA-376c-3p was previous reported to have a crucial role in the progression of human cancer. This study was aimed to investigate the influence of microRNA-376c-3p on the proliferation and migration of human gastric cancer cells and the associated mechanism. We explored the expression of microRNA-376c-3p in gastric cancer cells using reverse transcription-quantitative polymerase chain reaction. Also, we analyzed the association and biological significance of microRNA-376c-3p and SYF2 pre-mRNA-splicing factor in gastric cancer. MicroRNA-376c-3p expression was found downregulated in gastric cancer cell lines compared to the normal cell line. MicroRNA-376c-3p directly targeted SYF2 and reduced SYF2 expression. Overexpression of microRNA-376c-3p inhibits gastric cancer cell proliferation and migration. Besides that, overexpression of SYF2 abrogates the inhibitory influences on gastric cancer cell behaviors caused by microRNA-376c-3p mimic. These results showed that microRNA-376c-3p inhibits the proliferation and migration of gastric cancer cells via targeting SYF2.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Influence of miR-376c-3p/SYF2 Axis on the Progression of Gastric Cancer

Liu

Zhang

et al. 2019

Technol Cancer Res Treat

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“…As a prevalent tumor in women worldwide, the incidence of breast cancer accounts for 29% of all cancers and poses a severe health problem in terms of severe mortality and morbidity . In spite of considerable improvements in therapy, both outcome and prognosis are still barely satisfactory . Breast cancer cells exhibit elevated proliferative capacity, enhanced invasive and metastatic characteristics, and more seriously, develop the drug resistance during tumor progression.…”

Section: Introductionmentioning

confidence: 99%

“…1,2 In spite of considerable improvements in therapy, both outcome and prognosis are still barely satisfactory. 3 Breast cancer cells exhibit elevated proliferative capacity, enhanced invasive and metastatic characteristics, and more seriously, develop the drug resistance during tumor progression. There is a clear consensus that drug resistance of breast cancer is the main obstacle to the improvement of chemotherapy.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐221 promotes breast cancer resistance to adriamycin via modulation of PTEN/Akt/mTOR signaling

Yin

Wang

et al. 2020

Cancer Medicine

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As a prevalent tumor among women, breast cancer is still an incurable disease due to drug resistance. In this study, we report microRNA‐221 to have a significant effect on breast cancer resistance to adriamycin. The microRNA‐221 is elevated in tumor tissue compared with nearby nontumor samples, as well as in breast cancer cell line with adriamycin resistance (MCF‐7/ADR) compared to its parental line (MCF‐7) and the normal breast epithelial cell line (MCF‐10A). Enforced level of microRNA‐221 promotes cancer resistance to adriamycin, which in turn sustains cell survival and exacerbates malignant formation. Reciprocally, the silence of microRNA‐221 in cancer cells augments the sensitivity to chemotherapy, thereby resulting in enhanced apoptosis of MCF‐7/ADR cells. Mechanistically, we identify PTEN as a direct target of microRNA‐221, which was conversely associated with a microRNA‐221 level in breast tumors. The knock‐down of PTEN partially reversed the stimulatory role of microRNA‐221 in the modulation of the Akt/mTOR signaling. Taken together, these findings suggest microRNA‐221 suppresses PTEN transcription and activates Akt/mTOR pathway, which in turn enhances breast cancer resistance to adriamycin and promotes cancer development. Our data thus illuminate the microRNA‐221/PTEN axis may act as a promising strategy for the treatment of chemotherapy‐resistant breast tumors.

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“…Additionally, the defects of tumor suppressor genes such as ATM and TP53 of the P53 signaling pathways are also at the pivot point of the colorectal tumorigenesis [61,62]. In addition, the CALM2, SHISA4, RSPO2 , and SYF2 contributed to cell proliferation [63,64,65,66,67]. However, the role of these genes in the cancer development mechanism has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

Genetic Aberration Analysis in Thai Colorectal Adenoma and Early-Stage Adenocarcinoma Patients by Whole-Exome Sequencing

Intarajak

Udomchaiprasertkul

Bunyoo

et al. 2019

Cancers

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Colorectal adenomas are precursor lesions of colorectal adenocarcinoma. The transition from adenoma to carcinoma in patients with colorectal cancer (CRC) has been associated with an accumulation of genetic aberrations. However, criteria that can screen adenoma progression to adenocarcinoma are still lacking. This present study is the first attempt to identify genetic aberrations, such as the somatic mutations, copy number variations (CNVs), and high-frequency mutated genes, found in Thai patients. In this study, we identified the genomic abnormality of two sample groups. In the first group, five cases matched normal-colorectal adenoma-colorectal adenocarcinoma. In the second group, six cases matched normal-colorectal adenomas. For both groups, whole-exome sequencing was performed. We compared the genetic aberration of the two sample groups. In both normal tissues compared with colorectal adenoma and colorectal adenocarcinoma analyses, somatic mutations were observed in the tumor suppressor gene APC (Adenomatous polyposis coli) in eight out of ten patients. In the group of normal tissue comparison with colorectal adenoma tissue, somatic mutations were also detected in Catenin Beta 1 (CTNNB1), Family With Sequence Similarity 123B (FAM123B), F-Box And WD Repeat Domain Containing 7 (FBXW7), Sex-Determining Region Y-Box 9 (SOX9), Low-Density Lipoprotein Receptor-Related Protein 5 (LRP5), Frizzled Class Receptor 10 (FZD10), and AT-Rich Interaction Domain 1A (ARID1A) genes, which are involved in the Wingless-related integration site (Wnt) signaling pathway. In the normal tissue comparison with colorectal adenocarcinoma tissue, Kirsten retrovirus-associated DNA sequences (KRAS), Tumor Protein 53 (TP53), and Ataxia-Telangiectasia Mutated (ATM) genes are found in the receptor tyrosine kinase-RAS (RTK–RAS) signaling pathway and p53 signaling pathway, respectively. These results suggest that APC and TP53 may act as a potential screening marker for colorectal adenoma and early-stage CRC. This preliminary study may help identify patients with adenoma and early-stage CRC and may aid in establishing prevention and surveillance strategies to reduce the incidence of CRC.

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Overexpression of SYF2 promotes cell proliferation and correlates with poor prognosis in human breast cancer

Cited by 13 publications

References 26 publications

RETRACTED: Influence of miR-376c-3p/SYF2 Axis on the Progression of Gastric Cancer

RETRACTED: Influence of miR-376c-3p/SYF2 Axis on the Progression of Gastric Cancer

MicroRNA‐221 promotes breast cancer resistance to adriamycin via modulation of PTEN/Akt/mTOR signaling

Genetic Aberration Analysis in Thai Colorectal Adenoma and Early-Stage Adenocarcinoma Patients by Whole-Exome Sequencing

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