scholarly journals Combination of cisplatin, Hedyotis corymbosa L. and Tinospora crispa extracts as a new therapy for breast cancer cells 4T1 through in vitro induction and cell cycle modulation

Pharmaciana ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 107
Author(s):  
Rollando Rollando ◽  
Muhammad Hilmi Afthoni
2015 ◽  
Vol 12 (2) ◽  
pp. 55-59
Author(s):  
Edy Meiyanto

As chemotherapeutic backbone for breast cancer therapy, doxorubicin showed various side effects and induced resistancy of breast cancer cells. Development of targeted therapy on breast cancer focused on combinatorial therapy of doxorubicin and molecular targeted agents. PGV-0 and PGV-1, a curcumin analogue showed potency as co-chemotherapeutic agent with doxorubicin. Our previous study of PGV-0 and PGV-1 showed cytotoxic activity in T47D cells. Therefore, the aim of this research is to examine the synergistic effect of PGV-0, PGV-1 on the cytotoxic activity of doxorubicin through cell cycle modulation and apoptotic induction on MCF-7 breast cancer cell lines. The cytotoxic assay of PGV-0, PGV-1, doxorubicin, and their combination were carried out by using MTT assay. Cell cycle distribution and apoptosis were determined by flowcytometer FACS-Calibur and the flowcytometry data was analyzed using Cell Quest program. Single treatment of PGV-0, PGV-1 and doxorubicin showed cytotoxic effect on MCF-7 with cell viability IC50 value 50 µM, 6 µM and 350 nM respectively. Single treatment of Doxorubicin 175 nM induced G2/M arrest. Single treatment of PGV-0 5 µM induced G2/M arrest while in higher dose 12.5  µM, PGV-0 induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 5 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 12.5 µM also increased apoptosis induction. Single treatment of PGV-1 0.6 µM induced G1 arrest while in higher dose 1.5  µM, PGV-1 induced apoptosis. Combination of doxorubicin 175 nM and PGV-1 0.6 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 1.5 µM also increased apoptosis induction. PGV-0 and PGV-1 are potential to be delevoped as co-chemotherapeutic agent for breast cancer by inducing apoptosis and cell cycle modulation, but the molecular mechanism need to be explored detail.  Key words: PGV-0, PGV-1, doxorubicin, co-chemotherapy, breast cancer, cell cycle arrest, apoptosis


2019 ◽  
Vol 4 (44) ◽  
pp. 12971-12977
Author(s):  
Nenad Marković ◽  
Milan Zarić ◽  
Marija D. Živković ◽  
Snežana Rajković ◽  
Ivan Jovanović ◽  
...  

Author(s):  
Rollando Rollando

Objective: Ursolic acid was a compound found in Hedyotis corymbosa L., (HCoL) while berberine found in Tinospora crispa (TCa) which are proven to have cytotoxic effect to cancer cells. This research aims to review the effect of cisplatin, ethanolic extract of HCoL and TCa to the sensitivity increase on breast cancer cells, which will be confirmed through apoptosis induction and cell cycle modulation.Methods: The cytotoxic effect was tested using 3-(4,5-dimethylthiazol-2-il)-2,5-diphenyltetrazolium bromide assay on T47D cell using the IC50 parameter. The combination was tested by determining their combination index (CI) and cell viability. The combination effect of apoptosis induction and cell cycle modulation was observed using flow cytometry method.Results: The cytotoxic test result of the combination shows CI value of below 1 at the concentration of HCoL ethanolic extract as much as 1 μg/mL, TCa ethanolic extract as much as 6 μg/mL, and cisplatin as much as 2,5 μM. The combination of HCoL ethanolic extract, TCa ethanolic extract, and cisplatin results in phase S cell accumulation (29.98%) on breast cancer cell T47D and was able to induce apoptosis.Conclusion: The result proves that ethanolic extract of HCoL and TCa can be developed as a cochemotherapeutic agent with cisplatin to increase the effectivity of breast cancer treatment.


Oncotarget ◽  
2018 ◽  
Vol 9 (68) ◽  
pp. 33050-33050 ◽  
Author(s):  
Bhimashankar Gurushidhappa Utage ◽  
Milind Shivajirao Patole ◽  
Punam Vasudeo Nagvenkar ◽  
Sonali Shankar Kamble ◽  
Rajesh Nivarti Gacche

Oncotarget ◽  
2018 ◽  
Vol 9 (54) ◽  
pp. 30304-30323 ◽  
Author(s):  
Bhimashankar Gurushidhappa Utage ◽  
Milind Shivajirao Patole ◽  
Punam Vasudeo Nagvenkar ◽  
Sonali Shankar Kamble ◽  
Rajesh Nivarti Gacche

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4504
Author(s):  
Vaiyapuri Subbarayan Periasamy ◽  
Anvarbatcha Riyasdeen ◽  
Venugopal Rajendiran ◽  
Mallayan Palaniandavar ◽  
Hanumanthappa Krishnamurthy ◽  
...  

This research was aimed at finding the cytotoxic potential of the mixed ligand copper(II) complex [Cu(tdp)(phen)](ClO4)—where H(tdp) is the tetradentate ligand 2-[(2-(2-hydroxyethylamino)-ethylimino)methyl]phenol, and phen is 1,10-phenanthroline—to two genotypically different breast cancer cells, MCF-7 (p53+ and ER+) and MDA-MB-231 (p53- and ER-). The complex has been already shown to be cytotoxic to ME180 cervical carcinoma cells. The special focus in this study was the induction of cell death by apoptosis and necrosis, and its link with ROS. The treatment brought about nuclear fragmentation, phosphatidylserine externalization, disruption of mitochondrial trans-membrane potential, DNA damage, cell cycle arrest at sub-G1 phase, and increase of ROS generation, followed by apoptotic death of cells during early hours and a late onset of necrosis in the cells surviving the apoptosis. The efficacy of the complex against genotypically different breast cancer cells is attributed to a strong association through p53-mitochondrial redox—cell cycle junction. The ADMET properties and docking of the complex at the active site of Top1 are desirable attributes of a lead molecule for development into a therapeutic. Thus, it is shown that the copper(II)–phenolate complex[Cu(tdp)(phen)]+ offers potential to be developed into a therapeutic for breast cancers in general and ER-negative ones in particular.


2017 ◽  
Vol 41 (4) ◽  
pp. 1633-1648 ◽  
Author(s):  
Sumei Gao ◽  
Xiaoyan Li ◽  
Xia Ding ◽  
Wenwen Qi ◽  
Qifeng Yang

Background: Cepharanthine (CEP) is a biscoclaurine alkaloid extracted from Stephania cepharantha and has been shown to have an anti-tumour effect on different types of cancers. However, the anti-cancer effect of CEP on human breast cancer cells is still unclear. Methods: We used MTT, clone formation, in vitro scratch, invasion and migration assays to confirm the inhibitory role of CEP on the proliferation of breast cancer cells. Flow cytometry, plasmid construction and western blot analysis were used to study the detailed mechanisms. Results: Our study showed that CEP could inhibit cell proliferation by inducing autophagy, apoptosis, and G0/G1 cell cycle arrest of breast cancer cells. Furthermore, we found that CEP induced autophagy and apoptosis by inhibiting the AKT/mTOR signalling pathway. Conclusion: We found that CEP could inhibit growth and motility of MCF-7 and MDA-MB-231 breast cancer cell. Our study revealed an anti-tumour effect of CEP on breast cancer cells and suggests that CEP could be a potential new clinical therapy for breast cancer.


Homeopathy ◽  
2020 ◽  
Vol 109 (04) ◽  
pp. 198-206
Author(s):  
Sabiha Khan ◽  
Debadatta Nayak ◽  
Anil Khurana ◽  
Raj Kumar Manchanda ◽  
Chanderdeep Tandon ◽  
...  

Abstract Background Breast cancer is the second leading cause of cancer-related deaths in women. Conventional treatment such as chemotherapy, hormonal therapy and radiotherapy has decreased the mortality rate among cancer patients but has also revealed long-term side effects. Drug resistance and toxicity to normal cells compound the problems associated with the use of modern medicines. Hence, complementary or alternative treatment options are being explored. The current study, using different homeopathic potencies of Hydrastis canadensis, was conducted to distinguish between any effects they might have on hormone-dependent and independent breast cancer. Materials and Methods The cytotoxic effect of homeopathic medicine Hydrastis on hormone-dependent (MCF 7) and hormone-independent (MDA-MB-468) breast cancer cells was assessed using viability and colony-forming assays after 48 or 72 hours of treatment. Flow cytometry-based Annexin V-PI (propidium iodide), caspase 3 and cell cycle analysis was performed following treatment of cells with mother tincture or various potencies of Hydrastis (1C, 2C, 30C, 200C). Results Different potencies of Hydrastis displayed selective cytotoxic effects against MCF 7 cells, but only marginal effects against MDA-MB-468. The maximum cytotoxicity was established in the case of 1C following 72 hours of treatment. Treatment of breast cancer cells revealed an increase in the G0/G1 cell population, along with an increase in the caspase 3 levels and induction of apoptosis. Conclusion Hydrastis may have a selective cytotoxic effect against hormone-dependent breast cancer MCF 7 cells, leading to cell cycle arrest in the G0/G1 phase, which could be the plausible reason for the induction of apoptosis. The results need to be validated in vivo.


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