scholarly journals Retracted: Mukonal Inhibits Cell Proliferation, Alters Mitochondrial Membrane Potential and Induces Apoptosis and Autophagy in Human CNE1 Nasopharyngeal Carcinoma Cells

2021 ◽  
Vol 27 ◽  
Author(s):  
Yingyuan Guo ◽  
Yanru Hao ◽  
Guofang Guan ◽  
Shuaishuai Ma ◽  
Zhiling Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Membrane Potential ◽  
Nasopharyngeal Carcinoma ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Carcinoma Cells

scholarly journals K+/H+-antiporter nigericin arrests DNA synthesis in Ehrlich ascites carcinoma cells

1989 ◽  
Vol 86 (17) ◽  
pp. 6626-6629 ◽  
Author(s):  
L B Margolis ◽  
Y u Novikova I ◽  
I A Rozovskaya ◽  
V P Skulachev
Keyword(s):  
Membrane Potential ◽  
Dna Synthesis ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Low Concentrations ◽  
Ehrlich Ascites ◽  
Inhibition Of Dna Synthesis ◽  
Dna Synthesis Inhibition

Acidification of the cytoplasm of Ehrlich ascites carcinoma cells to pH 6.3 arrests DNA synthesis in these cells. Such an effect can be achieved by incubating the cells at pH 6.2 or by adding low concentrations of the K+/H+ antiporter, the antibiotic nigericin, at neutral pH. Glucose and anaerobiosis potentiate the nigericin effect. The inhibition of DNA synthesis by nigericin occurs without any significant decrease in the ATP concentration and in the mitochondrial membrane potential. The DNA synthesis inhibition is caused neither by a decrease in the intracellular [K+] nor by an increase in the intracellular [Na+] accompanying the nigericin effect (at least at low concentrations of the antibiotic). Nigericin should thus be regarded as a type of a cytostatic primarily affecting intracellular pH.

scholarly journals IFI35 is involved in the regulation of the radiosensitivity of colorectal cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yan Hu ◽  
Bing Wang ◽  
Ke Yi ◽  
Qingjun Lei ◽  
Guanghui Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Colony Formation ◽  
Mitochondrial Membrane ◽  
Luciferase Reporter ◽  
X Rays ◽  
Recombinant Interferon

Abstract Background Interferon regulatory factor-1 (IRF1) affects the proliferation of colorectal cancer (CRC). Recombinant interferon inducible protein 35 (IFI35) participates in immune regulation and cell proliferation. The aim of the study was to examine whether IRF1 affects the radiation sensitivity of CRC by regulating IFI35. Methods CCL244 and SW480 cells were divided into five groups: blank control, IFI35 upregulation, IFI35 upregulation control, IFI35 downregulation, and IFI35 downregulation control. All groups were treated with X-rays (6 Gy). IFI35 activation by IRF1 was detected by luciferase reporter assay. The GEPIA database was used to examine IRF1 and IFI35 in CRC. The cells were characterized using CCK-8, EdU, cell cycle, clone formation, flow cytometry, reactive oxygen species (ROS), and mitochondrial membrane potential. Nude mouse animal models were used to detect the effect of IFI35 on CRC. Results IRF1 can bind to the IFI35 promoter and promote the expression of IFI35. The expression consistency of IRF1 and IFI35 in CRC, according to GEPIA (R = 0.68, p < 0.0001). After irradiation, the upregulation of IFI35 inhibited cell proliferation and colony formation and promoted apoptosis and ROS, while IFI35 downregulation promoted proliferation and colony formation and reduced apoptosis, ROS, and mitochondrial membrane potential were also reduced. The in vivo experiments supported the in vitro ones, with smaller tumors and fewer liver metastases with IFI35 upregulation. Conclusions IRF1 can promote IFI35 expression in CRC cells. IFI35 is involved in the regulation of radiosensitivity of CRC cells and might be a target for CRC radiosensitization.

scholarly journals IFI35 is involved in the regulation of the radiosensitivity of colorectal cancer cells

2021 ◽  
Author(s):  
Yan Hu ◽  
Bing Wang ◽  
Ke Yi ◽  
Qingjun Lei ◽  
Guanghui Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Colony Formation ◽  
Mitochondrial Membrane ◽  
Luciferase Reporter ◽  
X Rays ◽  
Recombinant Interferon

Abstract Background: Interferon regulatory factor-1 (IRF1) affects the proliferation of colorectal cancer (CRC). Recombinant interferon inducible protein 35 (IFI35) participates in immune regulation and cell proliferation. The aim of the study was to examine whether IRF1 affects the radiation sensitivity of CRC by regulating IFI35.Methods: CCL244 and SW480 cells were divided into five groups: blank control, IFI35 upregulation, IFI35 upregulation control, IFI35 downregulation, and IFI35 downregulation control. All groups were treated with X-rays (6 Gy). IFI35 activation by IRF1 was detected by luciferase reporter assay. The GEPIA database was used to examine IRF1 and IFI35 in CRC. The cells were characterized using CCK-8, EdU, cell cycle, clone formation, flow cytometry, reactive oxygen species (ROS), and mitochondrial membrane potential. Nude mouse animal models were used to detect the effect of IFI35 on CRC.Results: IRF1 can bind to the IFI35 promoter and promote the expression of IFI35. The expression consistency of IRF1 and IFI35 in CRC, according to GEPIA (R = 0.68, p < 0.0001). After irradiation, the upregulation of IFI35 inhibited cell proliferation and colony formation and promoted apoptosis and ROS, while IFI35 downregulation promoted proliferation and colony formation and reduced apoptosis, ROS, and mitochondrial membrane potential were also reduced. The in vivo experiments supported the in vitro ones, with smaller tumors and fewer liver metastases with IFI35 upregulation.Conclusions: IRF1 can promote IFI35 expression in CRC cells. IFI35 is involved in the regulation of radiosensitivity of CRC cells and might be a target for CRC radiosensitization.

scholarly journals Rab11a Is Overexpressed in Gastric Cancer and Regulates FAK/AKT Signaling

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Jiang Du ◽  
Lin Fu ◽  
Jie Hao ◽  
Xiumin Lin ◽  
Qianze Dong
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Membrane Potential ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Mitochondrial Membrane Potential ◽  
Cell Lines ◽  
Mitochondrial Membrane ◽  
Akt Signaling ◽  
Gastric Cancers

Dysregulation of Rab11a has been implicated in the progression of several cancers. However, there have been no such studies for human gastric cancers. In the current study, we examined Rab11a protein expression and found it was upregulated in 49 of 108 gastric cancer tissues and correlated with local invasion, nodal metastasis, and advanced stage. Rab11a protein was higher in gastric cancer cell lines than normal gastric cell line. We transfected Rab11a plasmid and siRNA in both MGC803 and AGS cell lines. Rab11a overexpression increased the cell growth rate, colony numbers, and invasion ability in both MGC803 and AGS cell lines. Downregulation of Rab11a using siRNA decreased the cell proliferation rate, colony numbers, and inhibited invasion. Rab11a overexpression also conferred cisplatin resistance. Annexin V/PI staining showed that Rab11a overexpression suppressed cisplatin-induced apoptosis, while Rab11a depletion promoted cell apoptosis. We also showed that Rab11a overexpression maintained mitochondrial membrane potential. Western blot analysis revealed that Rab11a increased protein expression of MMP2, cyclin D1, Bcl-2, p-FAK, and p-AKT, while Rab11a depletion showed the opposite effects. Blockage of FAK using inhibitor downregulated Bcl-2, cyclin D1, MMP2, and p-AKT expression and abolished the effects of Rab11a on these proteins. In summary, our data demonstrated that Rab11a is upregulated in human gastric cancers. Rab11a facilitated cell proliferation and invasion, as well as cisplatin sensitivity and mitochondrial membrane potential, possibly via the FAK/AKT signaling pathway.

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