Effects of cyclin-dependent kinase 8 specific siRNA on the proliferation and apoptosis of colon cancer cells

Background: Colon cancer is one of the most common types of cancer worldwide. Multiple studies have unveiled the key role of microRNAs (miRNAs) in the development of various types of cancer. However, the mechanism of action of miR-125b in the development and progression of colon cancer remains unknown. Objective: In this study, we explored the association of miR-125b and signal transducer and activator of transcription 3 (STAT3) and its role in the proliferation and apoptosis of SW480 colon cancer cells. Methods: The miR-125b expression in NCM460, SW480, HT29, and HCT8 cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). SW480 cells were transfected with lentiviruses of GFP–miR–125b and GFP–NC to establish a stable miR-125b overexpression colon cancer cell model and a control model. The targeting relationship between miR-125b and STAT3 was analyzed using bioinformatics and verified by the dual-luciferase reporter gene assay. Cell proliferation and apoptosis were assessed using the Cell Counting Kit-8 assay and TUNEL staining. The expression levels of STAT3, Bcl-2, and Bax were analyzed using Western blot analysis. Results: It was found that the relative mRNA expression of miR-125b was decreased in SW480, HT29, and HCT8 cells compared with that in NCM460 cells (P<0.05). The luciferase reporter gene assay confirmed that miR-125b downregulated the STAT3 gene expression (P<0.05). Overexpression of miR-125b inhibited proliferation and promoted apoptosis in SW480 colon cancer cells and was accompanied by upregulated Bax expression and downregulated Bcl-2 expression (P<0.05). Re-expression of STAT3 promoted cell proliferation and inhibited cell apoptosis, whereas Bcl-2 expression increased, and Bax expression decreased (P<0.05). Conclusion: The miR-125b regulates the expression of Bax and Bcl-2 by downregulating the expression of STAT3, thereby inhibiting proliferation and inducing apoptosis of SW480 colon cancer cells.

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The Role of Interleukin-22 Receptor1 in the Proliferation and Apoptosis of Colonrectal Cancer

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2655 ◽

2021 ◽

Vol 11 (1) ◽

pp. 22-27

Author(s):

Xiaoning Qin ◽

Hongxun Ruan ◽

Yinghao Hao ◽

Weiqi Kong ◽

Jing Zhao ◽

...

Keyword(s):

Colorectal Cancer ◽

Colon Cancer ◽

Cancer Cells ◽

Colon Cancer Cells ◽

Interleukin 22 ◽

Nuclear Antigens ◽

Proliferation And Apoptosis ◽

Colorectal Cancer Cells ◽

Before And After ◽

And Control

Background: To study the relationship between interleukin-22 receptor1 (IL-22R1) and the proliferation and apoptosis of colon cancer cells. Methods: SW480, SW620 (Human Colorectal Cancer Cell Lines) that express positive to IL-22R1 were exposed in the environment of IL-22. The proliferation trial included 5 groups: IL-22, 5-FU, 5-FU + IL-22, medium and control. The apoptosis trial included 4 groups: IL-22, 5-FU, 5-FU + IL-22 and control. The result of apoptosis was detected by Apoptosis Kit (AnnxinVPE and 7-AAD), and proliferation was detected by Ki67 antibody (Cell proliferation-associated nuclear antigens). The rates of proliferation and apoptosis were detected by flow cytometry. Changes of the rate of proliferation and apoptosis before and after silencing were compared and analyzed statistically after silencing the gene of IL-22R1. Result: The combination of IL-22R1 and IL-22 could significantly inhibit the apoptosis of colon cancer cells and promote the proliferation of colon cancer cells (P < 0.05). The effect was significantly weakened when IL-22R1 was silenced (P < 0.05). Conclusion: IL-22R1 combined with IL-22 could promote the proliferation and inhibit apoptosis of colorectal cancer cells. In addition, blocking IL-22R1 could eliminate the influence of IL-22 on the proliferation and apoptosis of colorectal cancer cells.

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Effects of silk sericin on the proliferation and apoptosis of colon cancer cells

Biological Research ◽

10.4067/s0716-97602012000100006 ◽

2012 ◽

Vol 45 (1) ◽

pp. 45-50 ◽

Cited By ~ 38

Author(s):

Waraporn Kaewkorn ◽

Nanteetip Limpeanchob ◽

Waree Tiyaboonchai ◽

Sutatip Pongcharoen ◽

Manote Sutheerawattananonda

Keyword(s):

Colon Cancer ◽

Cancer Cells ◽

Colon Cancer Cells ◽

Silk Sericin ◽

Proliferation And Apoptosis

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Sulindac and sulindac sulfide alter the levels of pRb and p53 and the cyclin dependent kinase inhibitor p21 in HT-29 colon cancer cells

Gastroenterology ◽

10.1016/0016-5085(95)26215-6 ◽

1995 ◽

Vol 108 (4) ◽

pp. A475

Keyword(s):

Colon Cancer ◽

Cancer Cells ◽

Kinase Inhibitor ◽

Cyclin Dependent Kinase ◽

Colon Cancer Cells ◽

Cyclin Dependent Kinase Inhibitor ◽

Sulindac Sulfide ◽

Ht 29

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TGFβ/Smad3 regulates proliferation and apoptosis through IRS-1 inhibition in colon cancer cells

PLoS ONE ◽

10.1371/journal.pone.0176096 ◽

2017 ◽

Vol 12 (4) ◽

pp. e0176096 ◽

Cited By ~ 14

Author(s):

Katie L. Bailey ◽

Ekta Agarwal ◽

Sanjib Chowdhury ◽

Jiangtao Luo ◽

Michael G. Brattain ◽

...

Keyword(s):

Colon Cancer ◽

Cancer Cells ◽

Colon Cancer Cells ◽

Proliferation And Apoptosis

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Depletion of Mediator Kinase Module Subunits Represses Superenhancer-Associated Genes in Colon Cancer Cells

Molecular and Cellular Biology ◽

10.1128/mcb.00573-17 ◽

2018 ◽

Vol 38 (11) ◽

Cited By ~ 7

Author(s):

Emilia Kuuluvainen ◽

Eva Domènech-Moreno ◽

Elina H. Niemelä ◽

Tomi P. Mäkelä

Keyword(s):

Gene Expression ◽

Stem Cells ◽

Colon Cancer ◽

Cancer Cells ◽

Therapeutic Targets ◽

Cyclin Dependent Kinase ◽

Colon Cancer Cells ◽

Concomitant Decrease ◽

Oncogene Activation ◽

Myc Gene

ABSTRACT In cancer, oncogene activation is partly mediated by acquired superenhancers, which therefore represent potential targets for inhibition. Superenhancers are enriched for BRD4 and Mediator, and both BRD4 and the Mediator MED12 subunit are disproportionally required for expression of superenhancer-associated genes in stem cells. Here we show that depletion of Mediator kinase module subunit MED12 or MED13 together with MED13L can be used to reduce expression of cancer-acquired superenhancer genes, such as the MYC gene, in colon cancer cells, with a concomitant decrease in proliferation. Whereas depletion of MED12 or MED13/MED13L caused a disproportional decrease of superenhancer gene expression, this was not seen with depletion of the kinases cyclin-dependent kinase 9 (CDK8) and CDK19. MED12-MED13/MED13L-dependent superenhancer genes were coregulated by β-catenin, which has previously been shown to associate with MED12. Importantly, β-catenin depletion caused reduced binding of MED12 at the MYC superenhancer. The effect of MED12 or MED13/MED13L depletion on cancer-acquired superenhancer gene expression was more specific than and partially distinct from that of BRD4 depletion, with the most efficient inhibition seen with combined targeting. These results identify a requirement of MED12 and MED13/MED13L for expression of acquired superenhancer genes in colon cancer, implicating these Mediator subunits as potential therapeutic targets for colon cancer, alone or together with BRD4.

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