LDL cholesterol promotes the proliferation of prostate and pancreatic cancer cells by activating the STAT3 pathway
| Autor: | Arunachalam Chinnathambi, Young Yun Jung, Jae-Young Um, Jeong-Hyeon Ko, Sulaiman Ali Alharbi, Kwang Seok Ahn, Gautam Sethi |
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| Rok vydání: | 2020 |
| Předmět: |
Male
STAT3 Transcription Factor 0301 basic medicine Simvastatin Carcinogenesis Cell Survival Physiology Clinical Biochemistry 03 medical and health sciences chemistry.chemical_compound Prostate cancer 0302 clinical medicine Cell Movement Pancreatic tumor Cell Line Tumor Pancreatic cancer LNCaP Humans Medicine Viability assay RNA Small Interfering Pancreas Cell Proliferation business.industry Cholesterol Anticholesteremic Agents Prostate Prostatic Neoplasms Cancer Cholesterol LDL Janus Kinase 1 Cell Biology Janus Kinase 2 medicine.disease Gene Expression Regulation Neoplastic Pancreatic Neoplasms 030104 developmental biology chemistry 030220 oncology & carcinogenesis Cancer research RNA Interference lipids (amino acids peptides and proteins) business Signal Transduction Lipoprotein |
| Zdroj: | Journal of Cellular Physiology. 236:5253-5264 |
| ISSN: | 1097-4652 0021-9541 |
| Popis: | Hypercholesterolemia has been found to be closely linked with a significant increase in both cancer incidence and mortality. However, the exact correlation between serum cholesterol levels and cancer has not been completely deciphered. Here we analyzed the effect of low-density lipoprotein (LDL) cholesterol on prostate and pancreatic cancer cells. We noted that LDL induced a substantial STAT3 activation and JAK1, JAK2, Src activation in diverse prostate and pancreatic tumor cells. Moreover, LDL promoted cancer cell proliferation, migration, and invasion as well as upregulated the expression of diverse oncogenic gene products. However, deletion of LDL-activated STAT3 in LNCaP and PANC-1 cells and reduced LDL-induced cell viability. Simvastatin (SV) treatment also alleviated LDL-induced cell viability and migration ability in both the prostate and pancreatic tumor cells. These results demonstrate that LDL-induced STAT3 activation may exert a profound effect on the proliferation and survival of tumor cells. |
| Databáze: | OpenAIRE |
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