Cell-cycle dysregulation in breast cancer: breast cancer therapies targeting the cell cycle

Zafonte, Brian T.; Hulit, James; Amanatullah, Derek F.; Albanese, Chris; Wang, Chenguang; Rosen, Eliot M.; Reutens, Anne T.; Sparano, Joseph A.; Lisanti, Michael P.; Pestell, Richard G.

doi:10.2741/zafonte

Cited by 51 publications

(41 citation statements)

References 215 publications

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“…G1/S progression is tightly regulated by the pro-proliferative Cyclin D1 and CDK4 (17). Overexpression of Cyclin D1 and CDK4 is commonly detected in various types of cancer (18)(19)(20)(21). Consistent with the inhibitory effect of PZH on G1/S transition, our data indicated that PZH treatment suppressed the mRNA and protein expression of Cyclin D1 and CDK4 in Caco-2 cells.…”

Section: Pzh Regulates the Expression Of Cyclin D1 And Cdk4 Insupporting

confidence: 74%

“…G1/S progression is strongly regulated by Cyclin D1, which exerts its function by forming an active complex with its major catalytic partners, such as CDK4 (17). An unchecked or hyperactivated Cyclin D1/CDK4 complex often leads to uncontrolled cell division and malignancy (18)(19)(20)(21). Therefore, inhibiting excessive proliferation of tumor cells by blocking Cyclin D1/CDK4-mediated G1/S progression is one of the key approaches for the development of anticancer drugs.…”

Section: Introductionmentioning

confidence: 99%

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Pien Tze Huang inhibits the proliferation of human colon carcinoma cells by arresting G1/S cell cycle progression

Shen

Fu²,

Liu

et al. 2012

Oncology Letters

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Abstract. Pien Tze Huang (PZH), a well-known traditional Chinese formula prescribed 450 years ago in the Ming Dynasty, has been used in China and Southeast Asia for centuries as a folk remedy for various types of cancer, including colorectal cancer (CRC). Recently, we reported that PZH is capable of inhibiting colon cancer growth both in vivo and in vitro via the promotion of apoptosis and inhibition of tumor angiogenesis. To elucidate the mechanism of the tumoricidal activity of PZH, its effect on the proliferation of human colon carcinoma Caco-2 cells was evaluated and the underlying molecular mechanism was investigated. Results showed that PZH inhibited Caco-2 cell viability and survival in a dose-and/or time-dependent manner. In addition, PZH treatment was found to block the G1/S cell cycle progression. Moreover, PZH suppressed the mRNA and protein expression of pro-proliferative Cyclin D1 and CDK4. Findings of the present study suggest that inhibition of cell proliferation via the G1/S cell cycle arrest is a potential mechanism by which PZH can be effective in the treatment of cancer.

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Section: Pzh Regulates the Expression Of Cyclin D1 And Cdk4 Insupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Pien Tze Huang inhibits the proliferation of human colon carcinoma cells by arresting G1/S cell cycle progression

Shen

Fu²,

Liu

et al. 2012

Oncology Letters

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“…These data suggest that the CCND1 GA or AA genotype may augment the various influences of oestrogen in decreasing the risk of colorectal cancer and adenoma as well as increasing the risk of breast cancer. In previous studies, CCND1 can bind directly to the oestrogen receptor, transactivate oestrogen response elements (Zhou et al, 2001), and regulate oestrogen-dependent enhancer activity (Zafonte et al, 2000).…”

Section: Discussionmentioning

confidence: 89%

Cyclin D1 A870G polymorphism and the risk of colorectal cancer and adenoma

et al. 2006

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Cyclin D1 (CCND1) plays a key role in cell cycle control, particularly in the transition from G 1 to S phase, which is regulated by cyclindependent kinases. A common adenine to guanine polymorphism (A870G) in the CCND1 gene has been associated with a longer-life protein and an increased risk of colorectal cancer and adenoma in some studies. Among subjects with hereditary nonpolyposis colorectal cancer, the A870G polymorphism has also been associated with a younger age of onset of colorectal cancer. We analysed 181 colorectal cancer cases and 475 matched controls and 524 adenoma cases and 517 matched controls within women in the Nurses' Health Study (NHS) cohort, 171 colorectal cancer cases and 347 matched controls and 372 adenoma cases and 712 matched controls nested within men in the Health Professionals' Follow-Up Study (HPFS) cohort, and 258 colorectal cancer cases and 415 matched controls within men in the Physicians' Health Study (PHS) cohort to assess the risk associated with the CCND1 A870G genotype. Moreover, we assessed whether CCND1 genotype modified the effect of a sporadic (nonsyndromic) family history of colorectal cancer as well as the effect of other dietary and lifestyle risk factors for colorectal cancer and adenoma. In all cohorts combined, the CCND1 polymorphism did not show statistically significant associations to risk of colorectal cancer (odds ratio (OR) for A allele carriers, 1.04; 95% confidence interval (95% CI), 0.82 -1.32) or adenoma (OR, 0.96; 95% CI, 0.79 -1.18). The CCND1 A870G genotype was associated with a modest, although nonsignificantly elevated risk of colorectal cancer (OR, 1.59; 95% CI, 0.98 -2.57) in women. In contrast, the polymorphism was not associated with increased risk of adenoma in either men or women. Among participants with the A870G genotype, a family history of colorectal cancer conferred a substantially greater risk of colorectal cancer in the women (P for interaction ¼ 0.06) and adenoma in the men (P for interaction ¼ 0.02). Current postmenopausal hormone (PMH) use was associated with a significant reduction in the risk of colorectal cancer and adenoma among women with the A870G genotype, whereas there was no effect of PMH use among those with the GG genotype. The CCND1 polymorphism appeared to confer a modest elevation in the risk of colorectal cancer among women. Moreover, the A870G genotype may enhance the protective effect of postmenopausal oestrogen use on the development of colorectal neoplasia.

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“…A potential BRCA1-responsive element was localized to position À615 to À511 of the p27 KIP1 promoter. p27 KIP1 is thought to function as a tumor suppressor and to be a target for cell cycle dysregulation during mammary carcinogenesis (Zafonte et al, 2000). Thus, low p27 KIP1 expression in breast cancer specimens is correlated with histological aggressiveness and poor prognosis (Chiarle et al, 2001); and mice that are genetically heterozygous for p27 KIP1 show an increased susceptibility to tumorgenesis (Fero et al, 1998).…”

Section: Regulation Of Transcriptionmentioning

confidence: 99%

BRCA1 gene in breast cancer

Rosen

Fan

Pestell

et al. 2003

Journal Cellular Physiology

242

195

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The BRCA1 gene was identified and cloned in 1994 based on its linkage to early onset breast cancer and breast-ovarian cancer syndromes in women. While inherited mutations of BRCA1 are responsible for about 40-45% of hereditary breast cancers, these mutations account for only 2-3% of all breast cancers, since the BRCA1 gene is rarely mutated in sporadic breast cancers. However, BRCA1 expression is frequently reduced or absent in sporadic cancers, suggesting a much wider role in mammary carcinogenesis. Since BRCA1 was cloned in 1994, its molecular function has been the subject of intense investigation. These studies have revealed multiple functions of the BRCA1 that may contribute to its tumor suppressor activity, including roles in: cell cycle progression, several highly specialized DNA repair processes, DNA damage-responsive cell cycle checkpoints, regulation of a set of specific transcriptional pathways, and apoptosis. Many of these functions are linked to protein:protein interactions involving different portions of the 1,863 amino acid (aa) BRCA1 protein. BRCA1 functions in cell cycle progression and the DNA damage response appear to be regulated by distinct and specific phosphorylation events, but the molecular pathways activated by these phosphorylations are only beginning to be unraveled. In addition, the reason that BRCA1 mutation carriers develop specific tumor types (breast and ovarian cancers in women and possibly prostate cancers in men) is not clearly understood. Elucidation of the precise molecular functions of the BRCA1 gene product will greatly enhance our understanding of the pathogenesis of hereditary as well as sporadic mammary carcinogenesis.

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Cell-cycle dysregulation in breast cancer: breast cancer therapies targeting the cell cycle

Cited by 51 publications

References 215 publications

Pien Tze Huang inhibits the proliferation of human colon carcinoma cells by arresting G1/S cell cycle progression

Pien Tze Huang inhibits the proliferation of human colon carcinoma cells by arresting G1/S cell cycle progression

Cyclin D1 A870G polymorphism and the risk of colorectal cancer and adenoma

BRCA1 gene in breast cancer

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