Breast Cancer: Current Developments in Molecular Approaches to Diagnosis and Treatment

Mare, Jo‐Anne de la; Contu, Lara; Hunter, Morgan Campbell; Moyo, Buhle; Sterrenberg, Jason N.; Dhanani, Karim C.H.; Mutsvunguma, Lorraine Z.; Edkins, Adrienne L.

doi:10.2174/15748928113086660046

Cited by 68 publications

(48 citation statements)

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“…Human breast cancer cell line MCF-7 was provided by the School of Pharmacy, Jilin University (Jilin, China). MCF-7 was incubated in RPMI 1640 medium, which contained 10% fetal bovine serum, 100 U/l penicillin and 100 mg/ml streptomycin, at 37˚C in 5% CO 2 Chemicals and drugs. TPI was dissolved in DMSO to make a stock solution (40 mmol/l) and diluted to various concentrations with cell culture medium.…”

Section: Methodsmentioning

confidence: 99%

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Triptolide induces autophagy and apoptosis through ERK activation in human breast cancer MCF‑7 cells

et al. 2018

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Abstract.To investigate the effects of triptolide (TPI) on proliferation, autophagy and death in human breast cancer MCF-7 cells, and to elucidate the associated molecular mechanisms, intracellular alterations were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays. The results of the MTT assay revealed that TPI significantly reduced the MCF-7 cell survival rate when the concentration was >10 nmol/l. TPI activated a caspase cascade reaction by regulating Bcl-2-associated X protein (Bax), caspase-3 and B-cell lymphoma 2 expression, and promoted programmed cell death via the mitochondrial pathway. The results demonstrated that TPI significantly reduced the cell proliferation rate and viability in a time-and dose-dependent manner, which was confirmed by western blotting and immunofluorescent staining. TPI induced autophagy and influenced p38 mitogen-activated protein kinases, extracellular signal-regulated kinase (Erk)1/2, and mammalian target of rapamycin (mTOR) phosphorylation, which resulted in apoptosis. When cells were treated with a combination of TPI and the Erk1/2 inhibitor U0126, the downregulation of P62 and upregulation of Bax were inhibited, which demonstrated that the inhibition of Erk1/2 reversed the autophagy changes induced by TPI. The results indicated that Erk1/2 activation may be a novel mechanism by which TPI induces autophagy and apoptosis in MCF-7 breast cancer cells. In conclusion, TPI affects the proliferation and apoptosis of MCF-7 cells, potentially via autophagy and p38/Erk/mTOR phosphorylation. The present study offers a novel view of the mechanisms by which TPI regulates cell death.

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Section: Methodsmentioning

confidence: 99%

“…Prevention, early detection, and effective treatment are the key intervention points to increase the survival rate (1,2). About 1.7 million new breast cancer patients were diagnosed in 2012, representing approximately 12% of all cancer cases globally that year (3).…”

Section: Introductionmentioning

confidence: 99%

Triptolide induces autophagy and apoptosis through ERK activation in human breast cancer MCF‑7 cells

et al. 2018

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“…2 Although progress has been made in the diagnosis and treatment of breast cancer, the survival rate is still low. 3 Therefore, it is an emergency to investigate the underlying molecular mechanism of breast cancer and develop novel therapeutic targets for the treatment.…”

Section: Introductionmentioning

confidence: 99%

<p>FOXK1, Regulated by miR-365-3p, Promotes Cell Growth and EMT Indicates Unfavorable Prognosis in Breast Cancer</p>

Gao¹,

Tian²

2020

OTT

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Background: Forkhead box K1 (FOXK1) is members of the FOX transcription factor family. Previous work has found out that FOXK1 promotes cell proliferation, migration and invasion in several cancers, such as gastric cancer, glioma cancer and lung cancer; however, the exact role of FOXK1 in breast cancer is still poorly known. Methods: Here, the association between FOXK1 expression and the clinicopathological characteristics of patients with breast cancer was identified. To further decipher the functional roles of FOXK1, it was overexpressed or knocked down in MCF-7, MDA-MB-231 and MCF-10A cells. Cell Counting Kit-8, colony formation and cell cycle assays were performed to examine the proliferation of breast cancer cells. Moreover, wound-healing and Transwell invasion analyses were carried out to explore the effect of FOXK1 on breast cancer cell migration and invasion. Results: Our findings discovered that FOXK1 promotes cell proliferation, migration and invasion in breast cancer. In addition, consistent with the previous report, FOXK1 also facilitates EMT in breast cancer. TargetScan was used to predict upstream of FOXK1, indicating that miR-365-3p could regulate FOXK1 expression in breast cancer. Conclusion: The findings of the present study demonstrated that miR-365-3p-FOXK1 axis plays a key role in breast cancer.

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“…Breast cancer remains the most commonly diagnosed cancer in women worldwide [1, 2] and current therapies are plagued by the development of resistance and high toxicity [3]. Therefore, the best treatment approach would be to elucidate and employ strategies that effectively reduce the risk of breast cancer in women.…”

Section: Introductionmentioning

confidence: 99%

The serum protein profile of early parity which induces protection against breast cancer

et al. 2016

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Early parity reduces the risk of breast cancer in women while nulliparity and late parity increase the risk of breast cancer. In order to translate this protection to women where early pregnancy is not feasible, much work has focused on understanding how parity confers protection against breast cancer, the molecular mechanisms by which this occurs is still not well understood. Healthy parous and nulliparous women were recruited for this study. We assessed serum protein profiles of early parous, late parous, and nulliparous women using the Phospho Explorer antibody array. Significantly altered proteins identified were validated by Western blot analysis. In silico analysis was performed with the data obtained. Our findings indicate increased phosphorylation levels of CDK1, AKT1 and Epo-R increased cell cycle and cell proliferation in late/nulliparous women. Increased levels of LIMK1, paxillin, caveolin-1, and tyrosine hydroxylase in late/nulliparous women demonstrate enhanced cell stress while decreased activity of p-p53 and pRAD51 in late/nulliparous women indicates decreased apoptosis and increased genomic instability. Further, increased levels of pFAK, pCD3zeta, pSTAT5B, MAP3K8 in early parous women favor enhanced innate/adaptive immunity. Overall, we have identified a unique protein signature that is responsible for the decreased risk of breast cancer and these proteins can also serve as biomarkers to predict the risk of breast cancer.

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Breast Cancer: Current Developments in Molecular Approaches to Diagnosis and Treatment

Cited by 68 publications

References 0 publications

Triptolide induces autophagy and apoptosis through ERK activation in human breast cancer MCF‑7 cells

Triptolide induces autophagy and apoptosis through ERK activation in human breast cancer MCF‑7 cells

<p>FOXK1, Regulated by miR-365-3p, Promotes Cell Growth and EMT Indicates Unfavorable Prognosis in Breast Cancer</p>

The serum protein profile of early parity which induces protection against breast cancer

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