scholarly journals Dimethylfumarate Inhibits Colorectal Carcinoma Cell Proliferation: Evidence for Cell Cycle Arrest, Apoptosis and Autophagy

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1329 ◽  
Author(s):  
Kaluzki ◽  
Hailemariam-Jahn ◽  
Doll ◽  
Kaufmann ◽  
Balermpas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Carcinoma Cell ◽  
Human Colon ◽  
G1 Phase ◽  
Cycle Arrest

Recent studies have proven that Dimethylfumarate (DMF) has a marked anti-proliferative impact on diverse cancer entities e.g., on malignant melanoma. To explore its anti-tumorigenic potential, we examined the effects of DMF on human colon carcinoma cell lines and the underlying mechanisms of action. Human colon cancer cell line HT-29 and human colorectal carcinoma cell line T84 were treated with or without DMF. Effects of DMF on proliferation, cell cycle progression, and apoptosis were analyzed mainly by Bromodeoxyuridine (BrdU)- and Lactatdehydrogenase (LDH)assays, caspase activation, flowcytometry, immunofluorescence, and immunoblotting. In addition, combinational treatments with radiation and chemotherapy were performed. DMF inhibits cell proliferation in both cell lines. It was shown that DMF induces a cell cycle arrest in G0/G1 phase, which is accompanied by upregulation of p21 and downregulation of cyclin D1 and Cyclin dependent kinase (CDK)4. Furthermore, upregulation of autophagy associated proteins suggests that autophagy is involved. In addition, the activation of apoptotic markers provides evidence that apoptosis is involved. Our results show that DMF supports the action of oxaliplatin in a synergetic manner and failed synergy with radiation. We demonstrated that DMF has distinct antitumorigenic, cell dependent effects on colon cancer cells by arresting cell cycle in G0/G1 phase as well as activating both the autophagic and apoptotic pathways and synergizes with chemotherapy.

scholarly journals RASAL1 induces to downregulate the SCD1, leading to suppression of cell proliferation in colon cancer via LXRα/SREBP1c pathway

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Guangchuan Wang ◽  
Zhen Li ◽  
Xiao Li ◽  
Chunqing Zhang ◽  
Lipan Peng
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Cycle Arrest ◽  
Hct 116 ◽  
Scd1 Expression

Abstract Background Recent studies have confirmed that RASAL1 has an antitumor effect in many cancers, but its functional role and the molecular mechanism underlying in colon cancer has not been investigated. Results We collected human colon cancer tissues and adjacent non-tumor tissues, human colon cancer cell lines LoVo, CaCo2, SW1116, SW480 and HCT-116, and normal colonic mucosa cell line NCM460. RT-qPCR was used to detect the RASAL1 level in the clinical tissues and cell lines. In LoVo and HCT-116, RASAL1 was artificially overexpressed. Cell viability and proliferation were measured using CCK-8 assays, and cell cycle was detected via PI staining and flow cytometry analysis. RASAL1 significantly inhibited the cell proliferation via inducing cell cycle arrest, suppressed cell cycle associated protein expression, and decreased the lipid content and inhibited the SCD1 expression. Moreover, SCD1 overexpression induced and downregulation repressed cell proliferation by causing cell cycle arrest. Additionally, luciferase reporter assays were performed to confirm the direct binding between SREBP1c, LXRα and SCD1 promoter, we also demonstrated that RASAL1 inhibit SCD1 3′-UTR activity. RASAL1 inhibited tumor growth in xenograft nude mice models and shows inhibitory effect of SCD1 expression in vivo. Conclusion Taken together, we concluded that RASAL1 inhibited colon cancer cell proliferation via modulating SCD1 activity through LXRα/SREBP1c pathway.

scholarly journals Trichostatin A inhibits cell proliferation and induces cell cycle arrest in human esophageal carcinoma cell line EC1

2009 ◽  
Vol 17 (34) ◽  
pp. 3534
Author(s):  
Jun-Fen Ma ◽  
Ya-Nan Jiang ◽  
Ji-Min Zhao ◽  
You-Tian Huang ◽  
Ming-Yao Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Esophageal Carcinoma ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Carcinoma Cell ◽  
Trichostatin A ◽  
Carcinoma Cell Line ◽  
Cycle Arrest

Regenerating Gene 1B Silencing Inhibits Colon Cancer Cell HCT116 Proliferation and Invasion

2015 ◽  
Vol 30 (2) ◽  
pp. 217-225 ◽  
Author(s):  
Zhirong Liu ◽  
Yuehong Zhang ◽  
Jun Xie ◽  
Caiping Li ◽  
Xiaoxia Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Colorectal Carcinoma ◽  
Cell Cycle Arrest ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Cycle Arrest ◽  
Hct116 Cells

Background The human regenerating gene 1B ( REG1B) is found to be frequently up-regulated in many types of human tumors. It is unclear whether REG1B expression may have therapeutic value in colorectal carcinoma. Additionally, how REG1B is associated with the clinical features of colorectal carcinoma is not known. To investigate the relationship between REG1B and colorectal cancer, we analyzed REG1B expression in clinical specimens and cell lines and the effect of down-regulation of REG1B by short hairpin RNA (shRNA) in HCT116 cells. Methods Paraffin-embedded specimens from 30 pairs of colorectal cancer tissues and adjacent colon tissues were used to investigate the expression of REG1B by immunohistochemistry. We also examined whether REG1B itself may be related to cell proliferation, cell cycle arrest, apoptosis, migration and invasion in colon cancer HCT116 cells. Results Our results showed that REG1B was highly expressed in colorectal carcinoma and was significantly associated with cell differentiation status. The results also illustrated that REG1B silencing with shRNA inhibited cell proliferation, migration and invasion but did not induce apoptosis. Furthermore, down-regulation of REG1B induces G1-phase cell cycle arrest in colon cancer cells. Conclusions Knockdown of REG1B can inhibit cell proliferation, migration and invasion. It may act by a mechanism regulating cell cycle progression. Thus, REG1B may be a novel candidate therapeutic target for colorectal cancer.

Individual and Interactive Effects of Apigenin Analogs on G2/M Cell-Cycle Arrest in Human Colon Carcinoma Cell Lines

2004 ◽  
Vol 48 (1) ◽  
pp. 106-114 ◽  
Author(s):  
Weiqun Wang ◽  
Peter C. VanAlstyne ◽  
Kimberly A. Irons ◽  
She Chen ◽  
Jeanne W. Stewart ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carcinoma Cell ◽  
Human Colon ◽  
Interactive Effects ◽  
M Cell ◽  
Human Colon Carcinoma Cell ◽  
Cycle Arrest ◽  
Carcinoma Cell Lines ◽  
Human Colon Carcinoma
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