Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells

Wang, Ying; Wang, Leqiu; Yin, Changhao; An, B Z; Hao, Yankun; Wei, Tao; Li, Li; Song, Guanhua

doi:10.3892/mmr.2015.3558

Cited by 34 publications

(12 citation statements)

References 32 publications

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“…Studies have shown that ATO was an effective therapeutic agent in APL with 63.8 to 93% high remission rate and could prolong patients' survival rate (13). A number of studies also have revealed a pro-apoptotic activity of ATO in solid tumors, including breast cancer, gastric cancer, hepatocellular carcinomas and sarcoma (14)(15)(16)(17). Although ATO is able to improve the disease outcome, of note, ATO also introduces to common side effects such as gastrointestinal disorders, cough, fatigue, skin rash, myelosuppression and the most burden are the liver function failure and cardiac toxicity (18).…”

Section: Introductionmentioning

confidence: 99%

Combinatorial Low Dose Arsenic Trioxide and Cisplatin Exacerbates Autophagy via AMPK/STAT3 Signaling on Targeting Head and Neck Cancer Initiating Cells

Hu¹,

Teo²,

Huang

et al. 2020

Front. Oncol.

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Head and neck squamous cell carcinoma (HNSCC) is a highly lethal disease with high-level of epidemic both in the world and Taiwan. Previous studies support that head and neck cancer-initiating cells (HN-CICs), a subpopulation of cancer cells with enhanced stemness properties, contribute to therapy resistance and tumor recurrence. Arsenic trioxide (As 2 O 3 ; ATO) has shown to be an effective anti-cancer drug targeting acute promyelocytic leukemia (APL). Combinatorial treatment with high dose of ATO and cisplatin (CDDP) exert synergistic apoptotic effects in cancer cell lines of various solid tumors, however, it may cause of significant side effect to the patients. Nevertheless, none has reported the anti-cancerous effect of ATO/CDDP targeting HN-CICs. In this study, we aim to evaluate the low dose combination of ATO with conventional chemo-drugs CDDP treatment on targeting HN-CICs. We first analyzed the inhibitory tumorigenicity of co-treatment with ATO and chemo-drugs on HN-CICs which are enriched from HNSCC cells. We observed that ATO/CDDP therapeutic regimen successfully synergized the cell death on HN-CICs with a Combination Index (CI) <1 by Chou-Talalay's analysis in vitro. Interestingly, the ATO/CDDP regimen also induced exaggerated autophagy on HN-CICs. Additionally, this drug combination strategy also empowered both preventive and therapeutic effect by in vivo xenograft assays. Finally, we provide the underlying molecular mechanisms of ATO-based therapeutic regimen on HN-CICs. Together, low dose of combinatorial ATO/CDDP regimen induced cell death as well as exacerbated autophagy via AMPK-STAT3 mediated pathway in HN-CICs.

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Section: Introductionmentioning

confidence: 99%

Combinatorial Low Dose Arsenic Trioxide and Cisplatin Exacerbates Autophagy via AMPK/STAT3 Signaling on Targeting Head and Neck Cancer Initiating Cells

Hu¹,

Teo²,

Huang

et al. 2020

Front. Oncol.

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“…At low doses (0.01–1 μM), arsenic compounds increased proliferation of non‐tumorigenic MCF‐10A (As 2 O 3 ), and breast cancer MCF‐7 (As III ) cells . Conversely, at higher concentrations (∼5–10 μM), these compounds exerted apoptotic effects associated with accumulation of caspase enzymes, p21, growth arrest DNA‐damage‐inducible‐α GADD45 , and miR‐238 . These data pointed to chronic exposure as potentially important for transformation of normal breast epithelial cells, or growth of preneoplastic cells, as confirmed in prostate tissue in which As III triggered the transition to a steroid hormone‐independent phenotype .…”

Section: Resultsmentioning

confidence: 98%

Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds

Romagnolo

Daniels

Grunwald

et al. 2016

Molecular Nutrition Food Res

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Scope Reduced expression of tumor suppressor genes (TSG) increases the susceptibility to breast cancer. However, only a small percentage of breast tumors is related to family history and mutational inactivation of TSG. Epigenetics refers to non-mutational events that alter gene expression. Endocrine disruptors found in foods and drinking water may disrupt epigenetically hormonal regulation and increase breast cancer risk. This review centers on the working hypothesis that agonists of the aromatic hydrocarbon receptor (AHR); bisphenol A (BPA); and arsenic compounds, induce in TSG epigenetic signatures that mirror those often seen in sporadic breast tumors. Conversely, it is hypothesized that bioactive food components that target epigenetic mechanisms protect against sporadic breast cancer induced by these disruptors. Methods and results This review highlights 1) overlaps between epigenetic signatures placed in TSG by AHR-ligands, BPA, and arsenic with epigenetic alterations associated with sporadic breast tumorigenesis; and 2) potential opportunities for prevention of sporadic breast cancer with food components that target the epigenetic machinery. Conclusions Characterizing the overlap between epigenetic signatures elicited in TSG by endocrine disruptors with those observed in sporadic breast tumors may afford new strategies for breast cancer prevention with specific bioactive food components or diet.

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“…There is emerging evidence that ion channels play a role in many, and potentially all cancers. Therapeutics against voltage gated potassium channels have been shown in vivo to improve prognosis for glioblastoma and breast cancer (Arcangeli and Becchetti, 2017; Pointer et al, 2017; Wang et al, 2015), and there are studies implicating specific sodium (Brisson et al, 2011; Roger et al, 2015) and calcium channels (Phan et al, 2017; Qu et al, 2014) in cancers. We present strong evidence that the KCNQ family of genes also play a significant and functional role in human gastrointestinal cancers.…”

Section: Discussionmentioning

confidence: 99%

The Role of Potassium Channels in the Pathogenesis of Gastrointestinal Cancers and Therapeutic Potential

Shorthouse

Rahrmann

Kosmidou

et al. 2020

Preprint

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2 1 2 2 2 3 Short title: KCNQ genes in gastrointestinal cancer 2 4 2 SUMMARY 2 5 We present evidence that KCNQ genes are drivers and suppressors of 2 6 gastrointestinal (GI) cancer in humans. The KCNQ family of genes encode for 2 7 subunits of a potassium channel complex involved in membrane polarisation and 2 8little is known about their role in cancer. We use human cancer data and a 2 9 multidisciplinary computational-based approach including structural modelling and 3 0 simulation, coupled with in vitro experiments to show that KCNQ1 is a tumor 3 1 suppressor, and KCNQ3 and KCNQ5 are oncogenic across human GI cancers. We 3 2 link the expression of KCNQ genes to WNT signalling, EMT, and survival and 3 3

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Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells

Cited by 34 publications

References 32 publications

Combinatorial Low Dose Arsenic Trioxide and Cisplatin Exacerbates Autophagy via AMPK/STAT3 Signaling on Targeting Head and Neck Cancer Initiating Cells

Combinatorial Low Dose Arsenic Trioxide and Cisplatin Exacerbates Autophagy via AMPK/STAT3 Signaling on Targeting Head and Neck Cancer Initiating Cells

Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds

The Role of Potassium Channels in the Pathogenesis of Gastrointestinal Cancers and Therapeutic Potential

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