ABSTRACT
Objective: To investigate the effect of piperine on human breast cancer cells. Methods: The effect of piperine on proliferation and migration of human breast cancer cells, MCF-7 and MDA-MB-231, was investigated using colony formation assays, wound healing assays, Matrigel migration assays, flow cytometry, RT-qPCR, and Western blotting assays. Results: Piperine inhibited the growth of MCF-7 and MDA-MB-231 cells and suppressed colony formation. Cell reduction at the G 0 / G 1 phase and cell arrest at the G 2 /M phase were observed in breast cancer cells. However, the significant effect was only demonstrated in MDA-MB-231 cells. Moreover, cancer cell migration was suppressed by piperine at low concentration. RT-qPCR and Western blotting assays showed that piperine downregulated Rac1 gene and protein expression. Conclusions: Piperine could inhibit growth and migration of breast cancer cells by reducing Rac1 gene and protein expression.
ABSTRACT
Objective: To investigate the effect of piperine on human breast cancer cells. Methods: The effect of piperine on proliferation and migration of human breast cancer cells, MCF-7 and MDA-MB-231, was investigated using colony formation assays, wound healing assays, Matrigel migration assays, flow cytometry, RT-qPCR, and Western blotting assays. Results: Piperine inhibited the growth of MCF-7 and MDA-MB-231 cells and suppressed colony formation. Cell reduction at the G 0 / G 1 phase and cell arrest at the G 2 /M phase were observed in breast cancer cells. However, the significant effect was only demonstrated in MDA-MB-231 cells. Moreover, cancer cell migration was suppressed by piperine at low concentration. RT-qPCR and Western blotting assays showed that piperine downregulated Rac1 gene and protein expression. Conclusions: Piperine could inhibit growth and migration of breast cancer cells by reducing Rac1 gene and protein expression.
ABSTRACT
Background: Chemotherapeutic treatment of cholangiocarcinoma is largely ineffective, because it is due to non-responsive for the obscured reason of the cancer to anticancer agents. Study was to investigate the cytotoxicity effects of chemotherapeutic agents and curcumin in vitro.Objective: To test sensitivity of cholangiocarcinoma cell lines to chemotherapeutic agents and curcumin Material and Methods: Three cholangiocarcinoma (CCA) cell lines, including KKU-100, KKU-M214 and KKU-OCA17 were used in the study. All cell lines were treated with three chemotherapeutic agents (5-fluorouracil, doxorubicin and carboplatin) or curcumin. The cell viability was determined under a fluorescence microscope by counting the number of living and dead cells after treatment.Results: KKU-100 and KKU-M214 were the very sensitive cell lines to doxorubicin (IC50 values ranging from 0.4 to 0.7 nmol/l), whereas KKU-OCA17 was relatively more resistant cell line. Interestingly, all cell lines were sensitive to curcumin (IC50 values ranging from 3 to 17 μmol/l). Conclusion: This study showed different degrees of semsitivity of CCA cell lines to various chemotherapeutic agents. The data could serve as basic information for chemotherapeutic selection for the treatment in CCA patients. Moreover curcumin exhibits the cytotoxicity on CCA cell lines; thereby it is suggested to be very beneficial in the development of strategy for chemotherapy of CCA cancer.Keywords: cholangiocarcinoma, curcumin, chemotherapeutic agent
ABSTRACT
Cancer is the disease that mutilates patient life and family. Cancer chemotherapy is one of treatment modalities for some cancers and cancers in some stages. Current advances in chemotherapeutic drugs involve with the targeted drug therapy where it is distinct from the classical cytotoxic drugs which damage rapidly dividing cancer as well as normal cells. Target molecules of the new drugs include molecules in signaling pathways which confer advantages for growth, survival, metastasis, and resistance to dead signals from normal tissues or chemotherapeutic drugs. The target molecules of interest which undergo new drug development pipelines comprise various protein tyrosine kinases, i.e. epidermal growth factor family and vascular epidermal growth factor receptors; mitogen-activated protein kinases, and molecules involving in broad metabolic pathways, such as proteasomes, histone deacetylase and transcription factor proteins such as nuclear factor kappa B. The target molecules are derived from basic studies of cancer and evolved to be potential anticancer drugs. This new generation of targeting drugs offers an alternative of cancer chemotherapy and is also employed as potential research tools in cancer biology.