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4 results on '"Bangling Chen"'

1. Interleukin-1 receptor antagonist inhibits metastatic potential by down-regulating CXCL12/CXCR4 signaling axis in colorectal cancer

Author

Jiachi Ma, Wanqing Liang, Yaosheng Qiang, Lei Li, Jun Du, Chengwu Pan, Bangling Chen, Chensong Zhang, Yuzhong Chen, and Qingkang Wang

Subjects
Interleukin-1 receptor antagonist, CXCR4-CXCL12 axis, Colorectal cancer, Metastasis, Medicine, Cytology, QH573-671
Abstract

Abstract Background The aim of this study was to investigate the co-operative role of CXCR4/CXCL12 axis and IL-1Ra in metastatic processes mechanism by interactions between colorectal cancer cells and stromal cells in their microenvironment. Methods Expression of IL-1α, interleukin-1 receptor type I (IL-1 RI), CXCL12 and CXCR4 mRNA and proteins were determined by RT-PCR and Western blot. The effect of secreted level of CXCL12 by IL-1Ra on fibroblasts was measured by ELISA. CXCL12 regulate metastatic potential of colorectal cancer was evaluated by proliferation, invasion and angiogenesis assays, respectively, in which invasion and angiogenesis assays used an in vitro system consisting of co-cultured colorectal cells and stromal cells. Results IL-1α was expressed in high liver metastatic colorectal cancer cell lines (HT-29 and WiDr). The colorectal cancer cell-derived IL-1α and rIL-1α significantly promoted CXCL12 expression by fibroblasts, and this enhancing effect can be significantly inhibited by IL-1Ra (P

Published
2021
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2. Fibroblast-derived CXCL12 regulates PTEN expression and is associated with the proliferation and invasion of colon cancer cells via PI3k/Akt signaling

Author

Jiachi Ma, Xiaowen Sun, Yimin Wang, Bangling Chen, Liyu Qian, and Yaguo Wang

Subjects
Colorectal cancer, CXCL12/SDF-1α, PTEN, Proliferation, Invasiveness, Medicine, Cytology, QH573-671
Abstract

Abstract Background Stromal-derived CXCL12 play an important role which influence the proliferation and invasiveness of colon cancer in microenvironment. The present study aimed to analyze the underlying mechanism by which CXCL12 and tumour suppressor protein phosphatase and tensin homologue deleted on chromosome 10 (PTEN) influences the metastatic potential of colon cancer and internal relation of colon cancer and stromal cells. Methods RT-PCR and western blot were detected the expression of CXCL12, CXCR4 and PTEN in colon cancer cells and stromal cells. The co-operative effects of CXCL12 and PTEN on proliferation and invasion of colon cancer cells were evaluated by real-time PCR, proliferation and invasion assays using an in vitro system consisting of co-cultured cancer cells and stromal cells. We eventually investigated activation of PI3K/Akt signaling by CXCL12 regulate PTEN and involved in the metastatic process of colon cancer. In addition, we also examine how the knockdown of PTEN influences proliferation and invasion and correlate with CXCL12/CXCR4/PI3K/Akt, determination of PTEN up-down-stream targets that preferentially contribute to tumorigenesis. Results Blockage of PTEN phosphorylation led to a stronger enhancement of cell proliferation and invasion upon stimulation with CXCL12 via its activation of the PI3K/Akt signaling pathway. Furthermore, knockdown of PTEN by siRNA transfection was also found to enhance the activation of the PI3K/Akt pathway, thereby promoting cell invasion and proliferation. CXCL12 induced transcriptional down-regulation of activated PTEN and this signaling pathway promotes cell survival. CXCL12/CXCR4/PI3K/Akt cascade may be critical for colon cancer cells to metastasize. Conclusions Based on our results, we suggest that the modification of CXCR4, PTEN, or PI3K function might be promising new therapeutic approaches to inhibit the aggressive spread of colon cancer.

Published
2019
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3. Polyunsaturated Fatty Acids ω-3 and ω-6 Regulate the Proliferation Invasion and Angiogenesis of Human Gastric Cancer Through COX/PGE Signaling Pathway

Author

Bangling Chen, Yuzhong Chen, Chensong Zhang, Lei Li, Wanqing Liang, Jun Du, Chengwu Pan, Jiachi Ma, and Yuanpeng Wang

Subjects
chemistry.chemical_classification, genetic structures, Chemistry, Angiogenesis, Cancer research, medicine, Cancer, Signal transduction, medicine.disease, Polyunsaturated fatty acid
Abstract

Background: To investigate the effect of polyunsaturated fatty acids ω-3 and ω-6 and their metabolites prostaglandin PGE2 and PGE3 on the proliferation, invasion and neovascularization of gastric cancer.Methods: RT-PCR and ELISA were used to detect the gene and protein expression of COX-1 and COX-2 in gastric cancer cell lines, respectively. The effects of ω-3, ω-6, PFG2 and PEG3 on the proliferation, invasion and neovascularization of gastric cancer cells were detected by cell proliferation, invasion and neovascularization assay in vitro. COX-2 siRNA was synthesized by short gene interfering RNA (siRNA) technique and transfected into gastric cancer cells, and the expression of COX-2 protein in gastric cancer cell lines was detected again by Western blot. The effects of COX-2 gene silencing on proliferation, invasion and neovascularization of gastric cancer cells were detected by WST-1 assay, transwell chamber assay and gastric cancer neovascularization assay, respectively.Results: COX-2 was only expressed in MKN74 and MKN45 cell lines, while COX-1 was expressed in four gastric cancer cell lines. In gastric cancer cell lines with positive COX-2 expression, ω-6 and PEG2 could significantly enhance the proliferation, invasion and neovascularization of gastric cancer cells, and after transfection with COX-2 siRNA, the effects of ω-6 and PEG2 on enhancing the proliferation, invasion and neovascularization of gastric cancer cells were significantly attenuated; ω-3 and PEG3 could inhibit the proliferation, invasion and neovascularization of gastric cancer cells. In gastric cancer cell lines with negative COX-2 expression, ω-6 and PEG2 had no significant effect on the proliferation, invasion and neovascularization of gastric cancer; ω-3 and PEG3 could significantly inhibit the proliferation, invasion and neovascularization of gastric cancer.Conclusion: ω-6 PUFAs reinforce the metastatic potential energy of gastric cancer cells via COX-2/PGE2; ω-3 PUFAs inhibit the metastatic potential energy of gastric cancer via COX-1/PGE3.

Published
2021

4. Fibroblast-derived CXCL12 regulates PTEN expression and is associated with the proliferation and invasion of colon cancer cells via PI3k/Akt signaling

Author

Yimin Wang, Liyu Qian, Yaguo Wang, Xiaowen Sun, Bangling Chen, and Jiachi Ma

Subjects
PTEN, Stromal cell, Proliferation, lcsh:Medicine, Apoptosis, medicine.disease_cause, Biochemistry, 03 medical and health sciences, Phosphatidylinositol 3-Kinases, 0302 clinical medicine, medicine, Tensin, Humans, Neoplasm Invasiveness, RNA, Messenger, lcsh:QH573-671, RNA, Small Interfering, Molecular Biology, Protein kinase B, PI3K/AKT/mTOR pathway, 030304 developmental biology, Cell Proliferation, 0303 health sciences, biology, CXCL12/SDF-1α, lcsh:Cytology, Akt/PKB signaling pathway, Chemistry, Research, lcsh:R, PTEN Phosphohydrolase, Cell Biology, Fibroblasts, Colorectal cancer, Chemokine CXCL12, Invasiveness, Gene Expression Regulation, Neoplastic, 030220 oncology & carcinogenesis, Cancer cell, Colonic Neoplasms, biology.protein, Cancer research, Carcinogenesis, HT29 Cells, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

Background Stromal-derived CXCL12 play an important role which influence the proliferation and invasiveness of colon cancer in microenvironment. The present study aimed to analyze the underlying mechanism by which CXCL12 and tumour suppressor protein phosphatase and tensin homologue deleted on chromosome 10 (PTEN) influences the metastatic potential of colon cancer and internal relation of colon cancer and stromal cells. Methods RT-PCR and western blot were detected the expression of CXCL12, CXCR4 and PTEN in colon cancer cells and stromal cells. The co-operative effects of CXCL12 and PTEN on proliferation and invasion of colon cancer cells were evaluated by real-time PCR, proliferation and invasion assays using an in vitro system consisting of co-cultured cancer cells and stromal cells. We eventually investigated activation of PI3K/Akt signaling by CXCL12 regulate PTEN and involved in the metastatic process of colon cancer. In addition, we also examine how the knockdown of PTEN influences proliferation and invasion and correlate with CXCL12/CXCR4/PI3K/Akt, determination of PTEN up-down-stream targets that preferentially contribute to tumorigenesis. Results Blockage of PTEN phosphorylation led to a stronger enhancement of cell proliferation and invasion upon stimulation with CXCL12 via its activation of the PI3K/Akt signaling pathway. Furthermore, knockdown of PTEN by siRNA transfection was also found to enhance the activation of the PI3K/Akt pathway, thereby promoting cell invasion and proliferation. CXCL12 induced transcriptional down-regulation of activated PTEN and this signaling pathway promotes cell survival. CXCL12/CXCR4/PI3K/Akt cascade may be critical for colon cancer cells to metastasize. Conclusions Based on our results, we suggest that the modification of CXCR4, PTEN, or PI3K function might be promising new therapeutic approaches to inhibit the aggressive spread of colon cancer.

Published
2019

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