Induction of the mesenchymal to epithelial transition by demethylation- activated microRNA-200c is involved in the anti-migration/invasion effects of arsenic trioxide on human breast cancer cells

Si, Lu; Jiang, Fei; Li, Yuan; Ye, Xianqing; Mu, Juan; Wang, Xingxing; Ning, Shilong; Hu, Chunyan; Li, Zhong

doi:10.1002/mc.22157

Cited by 24 publications

(10 citation statements)

References 38 publications

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“…As demonstrated in our previous study, As 2 O 3 decreases the expressions of DNMT1, DNMT3a and DNMT3b, which epigenetically re‐expressed the functional estrogen receptor α in triple negative breast cancer (TNBC) cells, and sensitizes these cells to tamoxifen therapy . In addition, such a process is also involved in the upregulation of the miR‐200 family and miR‐491, which blocks the EMT and attenuates the migration and invasion potentials in TNBC and liver cancer cells . Previous studies indicate that miR‐155 is epigenetically silenced in human cancers .…”

Section: Discussionmentioning

confidence: 63%

“…(34) In addition, such a process is also involved in the upregulation of the miR-200 family and miR-491, which blocks the EMT and attenuates the migration and invasion potentials in TNBC and liver cancer cells. (8,35) Previous studies indicate that miR-155 is epigenetically silenced in human cancers. (19,20) Here, in the present study, the average methylation level of miR-155 promoter in PC-3 cells is 79.21%, while the average methylation level of miR-155 promoter in As 2 O 3 -treated PC-3 cells is 38.1%.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of transforming growth factor beta/SMAD signal by MiR‐155 is involved in arsenic trioxide‐induced anti‐angiogenesis in prostate cancer

Jiang

et al. 2014

Cancer Science

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Prostate cancer is the most common cause of cancer-related deaths in men. Current practices for treatment of prostate cancer are less than satisfactory because of metastasis and recurrence, which are primarily attributed to angiogenesis. Hence, anti-angiogenesis treatment is becoming a promising new approach for prostate cancer therapy. In addition to treating acute promyelocytic leukemia, arsenic trioxide (As2O3) suppresses other solid tumors, including prostate cancer. However, the effects of As2O3 on angiogenesis in prostate cancer cells, and the underlying molecular mechanisms remain unclear. In the present study, As2O3 attenuated angiogenic ability through microRNA-155 (miR-155)-mediated inhibition of transforming growth factor beta (TGF-β)/SMAD signal pathway in human prostate cancer PC-3 and LNCaP cells in vitro and in vivo. Briefly, As2O3 inhibited the activations/expressions of both TGFβ-induced and endogenous SMAD2/3. Furthermore, As2O3 improved the expression of miR-155 via DNA-demethylation. MiR-155, which targeted the SMAD2-3′UTR, decreased the expression and function of SMAD2. Knockdown of miR-155 abolished the As2O3-induced inhibitions of the TGF-β/SMAD2 signaling, the vascular endothelial growth factor secretion and angiogenesis. Through understanding a novel mechanism whereby As2O3 inhibits angiogenic potential of prostate cancer cells, our study would help in the development of As2O3 as a potential chemopreventive agent when used alone or in combination with other current anticancer drugs.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Inhibition of transforming growth factor beta/SMAD signal by MiR‐155 is involved in arsenic trioxide‐induced anti‐angiogenesis in prostate cancer

Jiang

et al. 2014

Cancer Science

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“…We found that CN-A alone could dose-dependently inhibit the invasion capacity of MDA-MB-231 cells. According to a recent report using Transwell assay (40), ATO also attenuated the invasion capacity of MDA-MB-231 cells in xCELLigence assay. Finally, we found that the combined treatment with CN-A and ATO markedly suppressed the invasion capacity (Fig.…”

Section: Discussionmentioning

confidence: 92%

Cotylenin A and arsenic trioxide cooperatively suppress cell proliferation and cell invasion activity in human breast cancer cells

Kasukabe

Okabe‐Kado

Kato

et al. 2014

International Journal of Oncology

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Abstract. Arsenic trioxide (ATO) is an approved treatment for acute promyelocytic leukemia (APL). It has also shown potential for treatment of multiple myeloma and various solid tumors including breast cancer. The requirement of high, toxic concentrations for the induction of apoptosis in non-APL and solid tumor cells is a major limitation for its use in other hematological malignancies and solid tumors. We have examined whether inducers of differentiation of leukemia cells can control the growth of solid tumor cells. In the present study, we found that cotylenin A, a plant growth regulator and a potent inducer of differentiation in myeloid leukemia cells, significantly potentiated both ATO-induced inhibition of cell growth in a liquid culture, and ATO-induced inhibition of anchorageindependent growth in a semi-solid culture in human breast cancer MCF-7 and MDA-MB-231 cells. ISIR-005 (a synthetic cotylenin A-derivative) was also able to enhance ATO-induced growth inhibition. The combined treatment with cotylenin A and ATO induced cleaved caspase-7 in MCF-7 cells at the concentrations which ATO alone scarcely induced and cotylenin A alone only weakly induced. Expression of survivin in MCF-7 cells was markedly decreased with the presence of both cotylenin A and ATO, although the expression of survivin was only slightly decreased by cotylenin A or ATO alone. The pretreatment with N-acetylcysteine significantly reduced the combination treatment-induced cell growth inhibition. These data suggest that induction of cleaved caspase-7, inhibition of survivin and oxidative responses are important events in the corporative inhibition in the growth of MCF-7 cells induced by both cotylenin A and ATO. Furthermore, we found that the combined treatment with cotylenin A and ATO also could be effective in suppressing the invasive capacity of MDA-MB-231 cells determined with the impedance-based xCELLigence Real-Time Cell Analysis technology. These results suggest that cotylenin A is an attractive enhancer for the ATO-induced anticancer activities in human breast cancer.

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“…A, Tumor volumes were calculated using the formula: induces the CSCs differentiation in pancreatic cancer, gliomas, glioblastoma, and HCC, in the molecular mechanisms, the blockage of signal transduction induced by Notch or GLI1 are involved Wu et al, 2013;Zhang et al, 2014;Zhen et al, 2010). In addition, As 2 O 3 modifies the expressions of a serial of miRNAs, such as miR-98, miR-30, miR-210, and miR-200 c, which are involved in the regulation of differentiation and self-renewal (Gao et al, 2014;Meng et al, 2011;Si et al, 2014;Yang et al, 2014). Here in our present study, exposure of HCC cells to As 2 O 3 decreased the CSCs-like properties effectively in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the Cancer Stem Cells-Like Properties by Arsenic Trioxide, Involved in the Attenuation of Endogenous Transforming Growth Factor Beta Signal

Jiang

Shen

et al. 2014

Toxicological Sciences

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The elevation of cancer stem cells (CSCs)-like properties is involved in the initiation and progression of various human cancers. Current standard practices for treatment of cancers are less than satisfactory because of CSCs-mediated recurrence. For this reason, targeting the CSCs or the cancer cells with CSCs-like properties has become the new approach for the cancer treatments. In addition to treating leukemia, arsenic trioxide (As₂O₃) also suppresses other solid tumors. However, the roles of As₂O₃ in the regulation of CSCs-like properties remain largely uninvestigated. Here by using sphere formation assay, luciferase reporter assay, and some other molecular biology approaches, we found that As₂O₃ attenuated the CSCs-like properties in human hepatocellular carcinoma (HCC). Briefly, in HCC cells and mice xenograft models, As₂O₃ improved the expression of miR-491 by DNA-demethylation. MiR-491, which targeted the SMAD3-3'-UTR, decreased the expressions of SMAD3, and inhibited the CSCs-like properties in HCC cells. Knockdown of either miR-491 or SMAD3 attenuated the As₂O₃-induced inhibition of endogenous transforming growth factor beta signal and the CSCs-like properties. Further, in HCC patients, miR-491 is inversely correlated with the expressions of SMAD3, CD133, and the metastasis/recurrence outcome. By understanding a novel mechanism whereby As₂O₃ inhibits the CSCs-like properties in HCC, our study would help in the design of future strategies of developing As₂O₃ as a potential HCC chemopreventive agent when used alone or in combination with other current drugs.

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Induction of the mesenchymal to epithelial transition by demethylation- activated microRNA-200c is involved in the anti-migration/invasion effects of arsenic trioxide on human breast cancer cells

Cited by 24 publications

References 38 publications

Inhibition of transforming growth factor beta/SMAD signal by MiR‐155 is involved in arsenic trioxide‐induced anti‐angiogenesis in prostate cancer

Inhibition of transforming growth factor beta/SMAD signal by MiR‐155 is involved in arsenic trioxide‐induced anti‐angiogenesis in prostate cancer

Cotylenin A and arsenic trioxide cooperatively suppress cell proliferation and cell invasion activity in human breast cancer cells

Inhibition of the Cancer Stem Cells-Like Properties by Arsenic Trioxide, Involved in the Attenuation of Endogenous Transforming Growth Factor Beta Signal

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