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SMC1 promotes proliferation and inhibits apoptosis through the NF??B signaling pathway in colorectal cancer.

ABSTRACT: Colorectal cancer (CRC) is the third most common cancer and a leading cause of cancer?associated mortality globally. Increasing evidence has indicated that structural maintenance of chromosomes 1 (SMC1) may serve an important role in solid tumors as a tumor enhancer. In the present study, it was identified via reverse transcription?quantitative PCR and western blot analyses that expression of SMC1 was significantly upregulated in CRC cell lines (SW480, HCT?116 and SW620) compared with NCM460 normal epithelial cells. To determine the potential involvement of SMC1 in the malignant phenotypes of CRC cells, SMC1 was knocked down in SW620 cells and SMC1 was overexpressed in SW480 cells in vitro. As a result, cell viability, proliferation, invasion and migration were suppressed in transduced SW620 cells but enhanced in SW480 cells, as determined using MTT, colony formation and Transwell assays; conversely, flow cytometric analysis revealed that cell apoptosis was increased in SW620 cells and inhibited in SW480 cells following lentiviral infection. In addition, an in vivo mouse xenograft model revealed that knocking down SMC1 suppressed tumor growth and increased apoptosis; however, overexpressing SMC1 enhanced tumor growth and suppressed apoptosis. Further experiments demonstrated that the role of SMC1 on CRC may involve downregulation of the NF??B?associated signaling pathway. Finally, the present data from clinical CRC tumor samples showed that increased expression of SMC1 was significantly associated with distant metastasis, higher TNM stage, primary tumor size, lymph node metastasis and worse overall survival. Collectively, the present results suggested that SMC1 served an important role in the development of CRC and may be a predictive prognostic biomarker in patients with CRC.

SUBMITTER: Li J

PROVIDER: S-EPMC6718103 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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SMC1 promotes proliferation and inhibits apoptosis through the NF‑κB signaling pathway in colorectal cancer.

Li Jin J He Jingdong J Wang Yuan Y Shu Yongqian Y Zhou Jianwei J

Oncology reports 20190808 4

Colorectal cancer (CRC) is the third most common cancer and a leading cause of cancer‑associated mortality globally. Increasing evidence has indicated that structural maintenance of chromosomes 1 (SMC1) may serve an important role in solid tumors as a tumor enhancer. In the present study, it was identified via reverse transcription‑quantitative PCR and western blot analyses that expression of SMC1 was significantly upregulated in CRC cell lines (SW480, HCT‑116 and SW620) compared with NCM460 nor ...[more]

PMID: 31524239

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Project description:Background: As a malignant tumor, pancreatic cancer is difficult to detect in its early stage. Pancreatic cancer progresses rapidly and has a short survival time. Most cases have metastasized to distant organs before diagnosis. The mechanism of induction of pancreatic cancer is not fully understood. Methods: In this study, bioinformatics predicted ATP binding cassette subfamily A member 12 (ABCA12) expression in pancreatic tissues and performed survival analysis, risk assessment, and enrichment analysis. The expression of ABCA12 in 30 pairs of clinical samples was detected by immunohistochemistry and we analyzed its correlation with clinical information. Both reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis were used to detect mRNA and protein expression in cell lines. Two different siRNAs and SW1990 cell line were used to construct pancreatic cancer cell models with ABCA12 knockdown. Cell viability was evaluated by cell counting kit-8 (CCK-8) and EdU proliferation assays. Wound healing assays and Transwell assays were used to measure the ability of cell migration and invasion. Flow cytometry was used to investigate the effect of ABCA12 on the proliferation cycle and apoptosis of pancreatic cancer. Western blot analysis detected changes in apoptosis, migration, and other pathway proteins in SW1990 cells after transfection. Results: ABCA12 is highly expressed in pancreatic cancer tissues and cells. After ABCA12 was knocked down, the proliferation, invasion, and migration of SW1990 cells were significantly reduced, and apoptosis was increased. The changes in pathway proteins suggested that ABCA12 may regulate the progression of pancreatic cancer through the AKT pathway. Conclusion: We found that ABCA12 is differentially expressed in pancreatic tissues and cells. ABCA12 can also affect the biological behavior of pancreatic cancer cells effectively, which may serve as a new target for pancreatic cancer diagnosis and treatment.

Dataset Information

SMC1 promotes proliferation and inhibits apoptosis through the NF??B signaling pathway in colorectal cancer.

Publications

SMC1 promotes proliferation and inhibits apoptosis through the NF‑κB signaling pathway in colorectal cancer.

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