Cell Cycle Regulatory Proteins in Breast Cancer: Molecular Determinants of Drug Resistance and Targets for Anticancer Therapies

Ahmad, Aamir; Wang, Zhiwei; Ali, Raza; Bitar, Bassam; Logna, Farah; Maitah, Ma'in Y.; Bao, Bin; Ali, Shadan; Kong, Dejuan; Li, Yiwei; Sarkar, Fazlul H.

doi:10.5772/24272

Cited by 9 publications

(12 citation statements)

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“…*p50.05, **p50.01. DOI: 10.3109/13880209.2014.931442 well as upregulation of cyclin-dependent kinase inhibitors (CDKIs) (Ahmad et al, 2012). Cyclin E/CDK2 and cyclin A/CDK2 complexes play an important role in G1-S transition and DNA replication, respectively.…”

Section: Discussionmentioning

confidence: 99%

Ethyl acetate extract fromGlycosmis parvaleaf induces apoptosis and cell-cycle arrest by decreasing expression of COX-2 and altering BCL-2 family gene expression in human colorectal cancer HT-29 cells

Buranabunwong

Ruangrungsi

Chansriniyom

et al. 2014

Pharmaceutical Biology

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Context: Glycosmis parva Craib (Rutaceae) is reported to have cytotoxic and anti-inflammatory activities by decreasing COX-2 expression. Objective: To investigate the effect of G. parva on human colorectal cancer cells expressing COX-2, HT-29 cells. Materials and methods: HT-29 cells were treated with ethyl acetate extract from the leaves of G. parva (GPE 6.25-100 mg/ml) for 24-72 h. Cell viability was evaluated by the resuzurin reduction assay. An apoptotic study was performed using annexinV/FITC-PI staining. The cellcycle pattern was investigated by PI staining. The expression of BCL-2 family genes was analyzed by quantitative RT-PCR and expression of cyclins and COX-2 were done by RT-PCR.Results: GPE at 6.25-100 mg/ml reduced HT-29 cell viability with IC 50 values of 69.49, 55.89, and 48.94 mg/ml at 24, 48, and 72 h, respectively. HT-29 apoptosis was induced by 18.23% at 100 mg/ml. Cells in S phase decreased by 5.22% and 13.28% at 50 and 100 mg/ml, respectively, causing G0/G1 (10.6% at 50 mg/ml) and G2/M (15.67% at 100 mg/ml) accumulation. GPE at 50 mg/ml downregulated cyclin A (11.46%), cyclin E (17.98%), BCL-2 (0.32-fold), and COX-2 (29.06%) expression with an increased BAK expression (1.79-fold). Discussion and conclusion: GPE reduced HT-29 cell viability, inhibited cell proliferation, induced apoptosis, and arrested the cell cycle. Underlying mechanisms may involve decreases in COX-2, cyclin A, and cyclin E expression in addition to changes in BCL-2 family gene expression. Fundamental knowledge of GPE anticancer effects found in this study could lead to future use of this compound for colorectal cancer treatment.

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Section: Discussionmentioning

confidence: 99%

Ethyl acetate extract fromGlycosmis parvaleaf induces apoptosis and cell-cycle arrest by decreasing expression of COX-2 and altering BCL-2 family gene expression in human colorectal cancer HT-29 cells

Buranabunwong

Ruangrungsi

Chansriniyom

et al. 2014

Pharmaceutical Biology

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“…The development of resistance to chemotherapy is considered a major hindrance to treatment of various cancers. Globally, decreased disease-free or overall survival (DFS/OS) is due mainly to recurrence and metastases of breast cancers in patients who do not http://etd.uwc.ac.za/ respond to targeted therapies from the start (de novo drug resistance) and even those who do respond to targeted therapies such as tamoxifen and trastuzumab and show signs of remission initially, only to turn refractory (relapse) to these treatments with time (acquired drug resistance [25][26][27][28][29][30][31][32]. Moreover, most chemotherapeutic drugs presently being used exhibit adverse side effects on the human body, namely, bleeding, hair loss, diarrhoea, and immunosuppression [33][34][35] which have negative impacts on the lives of affected patients [36][37][38][39][40][41][42].…”

Section: Problem Statementmentioning

confidence: 99%

“…The process of faithfully replicating the genetic information of a cell and its subsequent division into two daughter cells is known as the cell cycle [26,71,72,248]. The cell cycle can be envisioned as alternating cycles of interphase where the cell grows in size, synthesizes RNA and proteins, and replicates its DNA, and mitosis (M) where the newly replicated cell divides.…”

Section: The Cell Cyclementioning

confidence: 99%

“…Cancer cells exhibit deregulation of cell cycle and apoptosis and activation of oncogenic signal transduction pathway, resulting in abnormal proliferation [26,307,477,478]. The effects of FUC, CDDP, DOX and TAX alone or in combination on cell cycle distribution of MCF-7 and MCF-12A cells was determined by flow cytometry and showed alterations in Sub-G1, G0/G1, Data are means±SEM (n=3) representive of three independent experiments.…”

Section: And Mcf-12a Cellsmentioning

confidence: 99%

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Effects of Fucoidan and Chemotherapeutic Agent Combinations on Malignant and Non-malignant Breast Cell Lines

Abudabbus

Badmus

Shalaweh

et al. 2017

CPB

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Fucoidan is an effective antitumor agent, either alone or in combination with cisplatin, doxorubicin and taxol in MCF-7 breast cancer cells. Drug combinations that discriminate between cancerous and non-cancerous cells afford a plausible and viable strategy of attaining therapeutic efficacy and avoiding possible toxicity and side effects. These findings suggest that fucoidan is a promising candidate for cancer combination therapies.

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“…Many breast cancer patients do not respond to targeted therapies from the start, and this is called de novo drug resistance . A number of breast cancer patients, however, do respond to targeted therapies such as tamoxifen and trastuzumab and show signs of improvement initially, only to turn refractory to these treatments with the passage of time, called acquired resistance [5, 6]. Metastases as well as drug resistance phenotypes almost always result in poor prognosis and a disease condition that is progressively aggressive.…”

Section: Breast Cancer: the Problemmentioning

confidence: 99%

Pathways to Breast Cancer Recurrence

Ahmad

2013

ISRN Oncology

Self Cite

100

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Breast cancer remains a deadly disease, even with all the recent technological advancements. Early intervention has made an impact, but an overwhelmingly large number of breast cancer patients still live under the fear of “recurrent” disease. Breast cancer recurrence is clinically a huge problem and one that is largely not well understood. Over the years, a number of factors have been studied with an overarching aim of being able to prognose recurrent disease. This paper attempts to provide an overview of our current knowledge of breast cancer recurrence and its associated challenges. Through a survey of the literature on cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), various signaling pathways such as Notch/Wnt/hedgehog, and microRNAs (miRNAs), we also examine the hypotheses that are currently under investigation for the prevention of breast cancer recurrence.

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Cell Cycle Regulatory Proteins in Breast Cancer: Molecular Determinants of Drug Resistance and Targets for Anticancer Therapies

Cited by 9 publications

References 69 publications

Ethyl acetate extract fromGlycosmis parvaleaf induces apoptosis and cell-cycle arrest by decreasing expression of COX-2 and altering BCL-2 family gene expression in human colorectal cancer HT-29 cells

Ethyl acetate extract fromGlycosmis parvaleaf induces apoptosis and cell-cycle arrest by decreasing expression of COX-2 and altering BCL-2 family gene expression in human colorectal cancer HT-29 cells

Effects of Fucoidan and Chemotherapeutic Agent Combinations on Malignant and Non-malignant Breast Cell Lines

Pathways to Breast Cancer Recurrence

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