• Title, Summary, Keyword: breast cancer cell proliferation

Search Result 281, Processing Time 0.036 seconds

Anti-Proliferation Effects of Benzimidazole Derivatives on HCT-116 Colon Cancer and MCF-7 Breast Cancer Cell Lines

  • Al-Douh, Mohammed Hadi;Sahib, Hayder B.;Osman, Hasnah;Hamid, Shafida Abd;Salhimi, Salizawati M.
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.13 no.8
    • /
    • pp.4075-4079
    • /
    • 2012
  • Benzimidazoles 1-4 were obtained using modified synthesis methods and studied for their ability to inhibit cell proliferation of colon cancer cell HCT-116 and breast cancer cell MCF-7 using MTT assays. In the HCT-116 cell line, benzimidazole 2 was found to have an $IC_{50}$ value of $16.2{\pm}3.85{\mu}g/mL$ and benzimidazole 1 a value of $28.5{\pm}2.91{\mu}g/mL$, while that for benzimidazole 4 was $24.08{\pm}0.31{\mu}g/mL$. In the MCF-7 cell line, benzimidazole 4 had an $IC_{50}$ value of $8.86{\pm}1.10{\mu}g/mL$, benzimidazole 2 a value of $30.29{\pm}6.39{\mu}g/mL$, and benzimidazole 1 a value of $31.2{\pm}4.49{\mu}g/mL$. Benzimidazole 3 exerted no cytotoxity in either of the cell lines, with $IC_{50}$ values $>50{\mu}g/mL$. The results suggest that benzimidazoles derivatives may have chemotherapeutic potential for treatment of both colon and breast cancers.

ER81-shRNA Inhibits Growth of Triple-negative Human Breast Cancer Cell Line MDA-MB-231 In Vivo and in Vitro

  • Chen, Yue;Zou, Hong;Yang, Li-Ying;Li, Yuan;Wang, Li;Hao, Yan;Yang, Ju-Lun
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.13 no.5
    • /
    • pp.2385-2392
    • /
    • 2012
  • The lack of effective treatment targets for triple-negative breast cancers make them unfitted for endocrine or HER2 targeted therapy, and their prognosis is poor. Transcription factor ER81, a downstream gene of the HER2, is highly expressed in breast cancer lines, breast atypical hyperplasia and primary breast cancers including triple-negative examples. However, whether and how ER81 affects breast cancer carcinogenesis have remained elusive. We here assessed influence on a triple-negative cell line. ER81-shRNA was employed to silence ER81 expression in the MDA-MB-231 cell line, and MTT, colony-forming assays, and flow cytometry were used to detect cell proliferation, colony-forming capability, cell cycle distribution, and cell apoptosis in vitro. MDA-MB-231 cells stably transfected with ER81-shRNA were inoculated into nude mice, and growth inhibition of the cells was observed in vivo. We found that ER81 mRNA and protein expression in MDA-MB-231 cells was noticeably reduced by ER81-shRNA, and that cell proliferation and clonality were decreased significantly. ER81-shRNA further increased cell apoptosis and the residence time in $G_0/G_1$ phase, while delaying tumor-formation and growth rate in nude mice. It is concluded that ER81 may play an important role in the progression of breast cancer and may be a potentially valuable target for therapy, especially for triple negative breast cancer.

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

  • Zhou, Jing;Luo, Yan-Hong;Wang, Ji-Rong;Lu, Bin-Bin;Wang, Ke-Ming;Tian, Ye
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.12
    • /
    • pp.7601-7605
    • /
    • 2013
  • Background: Gambogenic acid is a major active compound of gamboge which exudes from the Garcinia hanburyi tree. Gambogenic acid anti-cancer activity in vitro has been reported in several studies, including an A549 nude mouse model. However, the mechanisms of action remain unclear. Methods: We used nude mouse models to detect the effect of gambogenic acid on breast tumors, analyzing expression of apoptosis-related proteins in vivo by Western blotting. Effects on cell proliferation, apoptosis and apoptosis-related proteins in MDA-MB-231 cells were detected by MTT, flow cytometry and Western blotting. Inhibitors of caspase-3,-8,-9 were also used to detect effects on caspase family members. Results: We found that gambogenic acid suppressed breast tumor growth in vivo, in association with increased expression of Fas and cleaved caspase-3,-8,-9 and bax, as well as decrease in the anti-apoptotic protein bcl-2. Gambogenic acid inhibited cell proliferation and induced cell apoptosis in a concentration-dependent manner. Conclusion: Our observations suggested that Gambogenic acid suppressed breast cancer MDA-MB-231 cell growth by mediating apoptosis through death receptor and mitochondrial pathways in vivo and in vitro.

Involvement of melastatin type transient receptor potential 7 channels in ginsenoside Rd-induced apoptosis in gastric and breast cancer cells

  • Kim, Byung Joo
    • Journal of Ginseng Research
    • /
    • v.37 no.2
    • /
    • pp.201-209
    • /
    • 2013
  • Ginsenoside, one of the active ingredients of Panax ginseng, has a variety of physiologic and pharmacologic effects. The purpose of this study was to explore the effects of ginsenoside Rd (G-Rd) on melastatin type transient receptor potential 7 (TRPM7) channels with respect to the proliferation and survival of AGS and MCF-7 cells (a gastric and a breast cancer cell line, respectively). AGS and MCF-7 cells were treated with different concentrations of G-Rd, and caspase-3 activities, mitochondrial depolarizations, and sub-G1 fractions were analyzed to determine if cell death occurred by apoptosis. In addition, human embryonic kidney (HEK) 293 cells overexpressing TRPM7 channels were used to confirm the role of TRPM7 channels. G-Rd inhibited the proliferation and survival of AGS and MCF-7 cells and enhanced caspase-3 activity, mitochondrial depolarization, and sub-G1 populations. In addition, G-Rd inhibited TRPM7-like currents in AGS and MCF-7 cells and in TRPM7 channel overexpressing HEK 293 cells, as determined by whole cell voltage-clamp recordings. Furthermore, TRPM7 overexpression in HEK 293 cells promoted G-Rd induced cell death. These findings suggest that G-Rd inhibits the proliferation and survival of gastric and breast cancer cells by inhibiting TRPM7 channel activity.

Fangchinoline Inhibits Cell Proliferation Via Akt/GSK-3beta/cyclin D1 Signaling and Induces Apoptosis in MDA-MB-231 Breast Cancer Cells

  • Wang, Chang-Dong;Yuan, Cheng-Fu;Bu, You-Quan;Wu, Xiang-Mei;Wan, Jin-Yuan;Zhang, Li;Hu, Ning;Liu, Xian-Jun;Zu, Yong;Liu, Ge-Li;Song, Fang-Zhou
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.15 no.2
    • /
    • pp.769-773
    • /
    • 2014
  • Fangchinoline (Fan) inhibits cell proliferation and induces apoptosis in several cancer cell lines. The effects of Fan on cell growth and proliferation in breast cancer cells remain to be elucidated. Here, we show that Fan inhibited cell proliferation in the MDA-MB-231 breast cancer cell line through suppression of the AKT/Gsk-3beta/cyclin D1 signaling pathway. Furthermore, Fan induced apoptosis by increasing the expression of Bax (relative to Bcl-2), active caspase 3 and cytochrome-c. Fan significantly inhibited cell proliferation of MDA-MB-231 cells in a concentration and time dependent manner as determined by MTT assay. Flow cytometry analysis demonstrated that Fan treatment of MDA-MB-231 cells resulted in cell cycle arrest at the G1 phase, which correlated with apparent downregulation of both mRNA and protein levels of both PCNA and cyclin D1. Further analysis demonstrated that Fan decreased the phosphorylation of AKT and GSK-3beta. In addition, Fan up-regulated active caspase3, cytochrome-c protein levels and the ratio of Bax/Bcl-2, accompanied by apoptosis. Taken together, these results suggest that Fan is a potential natural product for the treatment of breast cancer.

miR-485 Acts as a Tumor Suppressor by Inhibiting Cell Growth and Migration in Breast Carcinoma T47D Cells

  • Anaya-Ruiz, Maricruz;Bandala, Cindy;Perez-Santos, Jose Luis Martin
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.14 no.6
    • /
    • pp.3757-3760
    • /
    • 2013
  • MicroRNAs (miRNAs) are small, non-coding RNAs (18-25 nucleotides) that post-transcriptionally modulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. In this context, the present study aimed to evaluate the in vitro effects of miR-485 mimics in breast carcinoma T47D cells. Forty-eight hours after T47D cells were transfected with miR-485 mimics, an MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was utilized to determine the effects on cell viability. Colony formation and cell migration assays were adopted to determine whether miR-485 affects the proliferation rates and cell migration of breast carcinoma T47D cells. Our results showed that ectopic expression of miR-485 resulted in a significant decrease in cell growth, cell colony formation, and cell migration. These findings suggest that miR-485 might play an important role in breast cancer by suppressing cell proliferation and migration.

Hypoxia-Inducible Factor 1α Regulates the Transforming Growth Factor β1/ SMAD Family Member 3 Pathway to Promote Breast Cancer Progression

  • Peng, Jianheng;Wang, Xiaolin;Ran, Liang;Song, Junlong;Luo, Rong;Wang, Yonghong
    • Journal of Breast Cancer
    • /
    • v.21 no.3
    • /
    • pp.259-266
    • /
    • 2018
  • Purpose: The transforming growth factor ${\beta}1$ $(TGF-{\beta}1)/SMAD$ family member 3 (SMAD3) pathway, and hypoxia-inducible factor $1{\alpha}$ ($HIF-1{\alpha}$) are two key players in various types of malignancies including breast cancer. The $TGF-{\beta}1/SMAD3$ pathway can interact with $HIF-1{\alpha}$ in some diseases; however, their interaction in breast cancer is still unknown. Therefore, our study aimed to investigate the interactions between the $TGF-{\beta}1/SMAD3$ pathway and $HIF-1{\alpha}$ in breast cancer. Methods: Expression of $HIF-1{\alpha}$ in serum of breast cancer patients and healthy controls was detected by quantitative reverse transcription polymerase chain reaction, and the diagnostic value of $HIF-1{\alpha}$ for breast cancer was evaluated by receiver operating characteristic curve analysis. Breast cancer cell lines overexpressing SMAD3 and $HIF-1{\alpha}$ were established. Cell apoptosis and proliferation following different treatments were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, and cell counting kit-8, respectively. Expression of related proteins was detected by western blot. Results: Serum levels of $HIF-1{\alpha}$ were higher in breast cancer patients than in normal controls. Both SMAD3 and $HIF-1{\alpha}$ overexpression inhibited cell apoptosis and promoted cell proliferation. Treatment with inhibitors of $HIF-1{\alpha}$ and SMAD3 promoted apoptosis in breast cancer cells and inhibited their proliferation. Overexpression of $HIF-1{\alpha}$ promoted the expression of $TGF-{\beta}1$ and SMAD3, while SMAD3 overexpression did not significantly affect expression of $HIF-1{\alpha}$ or $TGF-{\beta}1$. Conclusion: $HIF-1{\alpha}$ serves as an upstream regulator of the $TGF-{\beta}1/SMAD3$ pathway and promotes the growth of breast cancer.

Effect of Cyclin D2 on Cell Proliferation in T-47D Breast Cancer Cells (인체 유방암 세포에서 과다발현 시킨 Cyclin D2의 영향에 대한 연구)

  • 김현준;이근수;전상학;공구
    • Environmental Mutagens and Carcinogens
    • /
    • v.24 no.1
    • /
    • pp.1-9
    • /
    • 2004
  • Three D-type cyelins (D1, D2, and D3) are expressed in G1 phase of the cell cyele and have been implicated in cell transformation and neoplasia in human and mouse. Cyclin D1 overexpression or amplification was described in various human cancers. However, there is controversy about the role of cyclin D2 in cell cyele progression and human carcinogenesis. Specially, loss of cyelin D2 is involved in a vital tumor suppressor function in normal breast tissue, and that its loss may be related to tumorigenesis. The author examined to effect over-expression of cyclin D2 on the cell proliferation, apoptosis, and cell cycle using cyclin D2 transfected stable T47D breast cancer cells to investigate whether cyclinD2 functions as a positive regulator or negative regulator in cell proliferation. Overexpression of cyclin D2 led to the suppression of cell growth in cyclin D2 transfected T47D in both in its expression level and a time dependent manner with up to 50% reduction of cell growth at 72 hours. Therefore, the authors performed the cell cycle phase analysis using the flow cytometry to investigate the effect of cyclin D2 on the cell cycle phase in cyclin D2 transfected stable T47D cells. The flow cytometry analysis revealed increased sub G0 phase in cyclin D2 transfeted cells up to 23% at 72 hours. To confirm these results induced by overexpression of cyclinD2, the apoptotic bodies were counted in control and cyclin D2 transfected T47 cells. There are markedly increases of apoptotic bodies in cyclin D2-transfected cells up to 18%. These results suggested that Cyclin D2 suppresses the cell proliferation in breast cancers cells via the induction of apotosis.

  • PDF

Anti-Cancer Effect of IN-2001 in MDA-MB-231 Human Breast Cancer

  • Min, Kyung-Nan;Joung, Ki-Eun;Kim, Dae-Kee;Sheen, Yhun-Yhong
    • Biomolecules & Therapeutics
    • /
    • v.20 no.3
    • /
    • pp.313-319
    • /
    • 2012
  • In recent years, inhibition of HDACs has emerged as a potential strategy to reverse aberrant epigenetic changes associated with cancer, and several classes of HDAC inhibitors have been found to have potent and specific anticancer activities in preclinical studies. But their precise mechanism of action has not been elucidated. In this study, a novel synthetic inhibitor of HDAC, 3-(4-dimethylamino phenyl)-N-hydroxy-2-propenamide [IN-2001] was examined for its antitumor activity and the underlying molecular mechanisms of any such activity on human breast cancer cell lines. IN-2001 effectively inhibited cellular HDAC activity ($IC_{50}$ = 0.585 nM) inMDA-MB-231 human breast cancer cells. IN-2001 caused a significant dose-dependent inhibition of cell proliferation in estrogen receptor (ER) negative MDA-MB-231human breast cancer cells. Cell cycle analysis revealed that the growth inhibitory effects of IN-2001 might be attributed to cell cycle arrest at $G_0/G_1$ and/or $G_2$/Mphase and subsequent apoptosis in human breast cancer cells. These events are accompanied by modulating several cell cycle and apoptosis regulatory genes such as CDK inhibitors $p21^{WAF1}$ and $p27^{KIP1}$ cyclin D1, and other tumor suppressor genes such as cyclin D2. Collectively, IN-2001 inhibited cell proliferation and induced apoptosis in human breast cancer cells and these findings may provide new therapeutic approaches, combination of antiestrogen together with a HDAC inhibitor, in the hormonal therapy-resistant ER-negative breast cancers. In summary, our data suggest that this histone deacetylase inhibitor, IN-2001, is a novel promising therapeutic agent with potent antitumor effects against human breast cancers.

Inhibition of proliferation of human breast cancer cell (SK-BR3) and liver cancer cell(SK-Hepl) in tissue culture by the CCCA from Cordyceps militaris

  • Lee, Seung-Jeong;Han, Shin-Ha;Park, Eun-Jung;Lee, Chong-Kil;You, Byeong-Jin;Cho, Kyung-Hee;Ha, Nam-Joo;Kim, Kyung-Jae
    • Proceedings of the PSK Conference
    • /
    • /
    • pp.140.1-140
    • /
    • 2003
  • Permanent cell culture lines derived from human cancer tissue are important experimental models in the study of human cancer cell proliferation. The in vitro effects of C. militaris and its extracted fractions on the human breast cancer (SK-BR3), liver cancer (SK-Hep1, HepG2), kidney cancer (p15), lymphoma (Jurkat) were studied. F1 (CCCA, crude cordycepin containing adenosine), F2 (ethanol precipitation), F3 (ethanol soluble supernatant) and F4 (fraction of through SK-1B) significantly stimulated in vitro cytotoxic in human cancer cell lines. (omitted)

  • PDF