Emerging Role of CaV1.2 Channels in Proliferation and Migration in Distinct Cancer Cell Lines

Oncology ◽  
2017 ◽  
Vol 93 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Gustavo Martínez-Delgado ◽  
Ricardo Felix
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals MicroRNA-23a promotes colorectal cancer cell migration and proliferation by targeting at MARK1

2019 ◽  
Vol 51 (7) ◽  
pp. 661-668 ◽  
Author(s):  
Xiaoli Tang ◽  
Meiyuan Yang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Daorong Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Functional Role ◽  
Expression Level ◽  
Colorectal Cancer Cell ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract The functional role of microRNA-23a in tumorigenesis has been investigated; however, the exact mechanism of microRNA-23a (miR-23a) in colorectal cancer development has not been fully explored. In the present study, we aimed to investigate the molecular functional role of miR-23a in colorectal carcinogenesis. Quantitative real-time polymerase chain reaction was conducted to investigate the expression level of miR-23a in tissue samples and cell lines (HCT116 and SW480). CCK-8, colony formation and Transwell assay were used to explore the role of miR-23a in cell proliferation and migration. Dual luciferase reporter assay was used to identify the direct binding of miR-23a with its target, MARK1. Western blot analysis was used to analyze the expression level of MARK1, as well as a confirmed miR-23a target gene, MTSS1, in miR-23a-mimic and miR-23a-inhibit groups. Rescue experiments were conducted by overexpression of MARK1 in miR-23a-mimic-transfected cell lines. The results showed that miR-23a was highly expressed in colorectal cancer tissue and cell lines. MiR-23a could promote proliferation and migration of colorectal cancer cell lines. MARK1 was a direct target of miR-23a and the expression level of MARK1 was down-regulated in miR-23a-mimic-transfected cell lines but up-regulated in miR-23a-inhibit-transfected cells. Overexpression of MARK1 could partly reverse the cancer-promoting function of miR-23a. Our results suggested that miR-23a promotes colorectal cancer cell proliferation and migration by mediating the expression of MARK1. MiR-23a may be a potential therapeutic target for colorectal cancer treatment.

scholarly journals MicroRNA-125b predicts clinical outcome and suppressed tumor proliferation and migration in human gallbladder cancer

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769224 ◽  
Author(s):  
Liang Yang ◽  
Sheng Huang ◽  
Hongbin Ma ◽  
Xiaoxiong Wu ◽  
Feiling Feng
Keyword(s):  
Gallbladder Cancer ◽  
Cancer Patients ◽  
Cell Lines ◽  
Cancer Cell ◽  
Clinical Stage ◽  
Cancer Cell Lines ◽  
Human Gallbladder ◽  
And Migration ◽  
Proliferation And Migration

We intended to investigate the functional role and clinical relevance of microRNA-125b in human gallbladder cancer. Quantitative real-time polymerase chain reaction was used to examine microRNA-125b expression in gallbladder cancer cell lines, and 79 pairs of gallbladder cancer and normal gallbladder clinical tissues. Clinical correlations between tumorous microRNA-125b expression and gallbladder cancer patients’ clinicopathological variances or overall survivals were statistically analyzed. In gallbladder cancer cell lines, TYGBK-8 and G-415 cells, microRNA-125b was upregulated to examine its regulatory effect on gallbladder cancer proliferation and migration in vitro. MicroRNA-125b was significantly downregulated in gallbladder cancer cell lines and human gallbladder cancer tumors. MicroRNA-125b in gallbladder cancer was significantly correlated with patients’ clinical stage, tumor differentiation, lymph metastasis, and tumor invasion. Low tumorous microRNA-125b expression was also found to be associated with poor overall survivals among gallbladder cancer patients. In vitro studies demonstrated that microRNA-125b upregulation significantly suppressed proliferation and migration in TYGBK-8 and G-415 cells. Tumorous microRNA-125b is an independent prognostic biomarker for patients with gallbladder cancer and possibly acts as a tumor suppressor in gallbladder cancer.

scholarly journals The effect of MTHFD2 on the proliferation and migration of colorectal cancer cell lines

2019 ◽  
Vol Volume 12 ◽  
pp. 6361-6370 ◽  
Author(s):  
Yameng Wei ◽  
Pengfei Liu ◽  
Qian Li ◽  
Juan Du ◽  
Yani Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cell Lines ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Human Telomerase Reverse Transcriptase as a Therapeutic Target of Dihydroartemisinin for Esophageal Squamous Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Qingrong Li ◽  
Qiang Ma ◽  
Lei Xu ◽  
Chuanli Gao ◽  
Lihua Yao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Telomerase Reverse Transcriptase ◽  
Squamous Cancer ◽  
And Migration ◽  
Esophageal Squamous Cancer ◽  
Proliferation And Migration

Objective: To elucidate the oncogenic role of human telomerase reverse transcriptase (hTERT) in esophageal squamous cancer and unravel the therapeutic role and molecular mechanism of dihydroartemisinin (DHA) by targeting hTERT.Methods: The expression of hTERT in esophageal squamous cancer and the patients prognosis were analyzed by bioinformatic analysis from TCGA database, and further validated with esophageal squamous cancer tissues in our cohort. The Cell Counting Kit-8 (CCK8) and colony formation assay were used to evaluate the proliferation of esophageal squamous cancer cell lines (Eca109, KYSE150, and TE1) after hTERT overexpression or treated with indicated concentrations of DHA. Transwell migration assay and scratch assay were employed to determine the migration abilities of cancer cells. Fluorescence microscopy and flow cytometry were conducted to measure the intracellular reactive oxygen species (ROS) levels in cancer cells after treated with DHA. Moreover, RT-PCR and Western blot were performed to test the alteration of associated genes on mRNA and protein level in DHA treated esophageal squamous cancer cell lines, respectively. Furthermore, tumor-bearing nude mice were employed to evaluate the anticancer effect of DHA in vivo.Results: We found that hTERT was significantly upregulated in esophageal squamous cancer both from TCGA database and our cohort also. Overexpression of hTERT evidently promoted the proliferation and migration of esophageal squamous cancer cells in vitro. Moreover, DHA could significantly inhibit the proliferation and migration of esophageal cancer cell lines Eca109, KYSE150, and TE1 in vitro, and significantly down-regulate the expression of hTERT on both mRNA and protein level in a time- and dose-dependent manner as well. Further studies showed that DHA could induce intracellular ROS production in esophageal cancer cells and down-regulate SP1 expression, a transcription factor that bound to the promoter region of hTERT gene. Moreover, overexpression of SP1 evidently promoted the proliferation and migration of Eca109 and TE1 cells. Intriguingly, rescue experiments showed that inhibiting ROS by NAC alleviated the downregulation of SP1 and hTERT in cells treated with DHA. Furthermore, overexpression of SP1 or hTERT could attenuate the inhibition effect of DHA on the proliferation and migration of Eca109 cells. In tumor-bearing nude mice model, DHA significantly inhibited the growth of esophageal squamous cancer xenografts, and downregulated the expression of SP1 and hTERT protein, while no side effects were observed from heart, kidney, liver, and lung tissues by HE stain.Conclusion: hTERT plays an oncogenic role in esophageal squamous cancer and might be a therapeutic target of DHA through regulating ROS/SP1 pathway.

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