Knockdown of the Bmi-1 oncogene inhibits cell proliferation and induces cell apoptosis and is involved in the decrease of Akt phosphorylation in the human breast carcinoma cell line MCF-7

Xu, Zhisheng; Liu, Hongtao; Lv, Xinquan; Liu, Yuqiong; Li, Shenglei; Li, Huixiang

doi:10.3892/or.2010.1078

Cited by 19 publications

(21 citation statements)

References 29 publications

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“…In agreement with published data [27], overexpression of Bmi-1 protein (Fig. 1c) led to a significant (1.6-fold) increase in MCF-7 cell viability (Fig.…”

Section: Resultssupporting

confidence: 93%

“…One study showed a decrease in cell viability in MCF-7 cells after knockdown of the Bmi-1 protein [27]. The present study reveals that while Bmi-1 expression affects MCF-7 cell viability (Fig.…”

Section: Discussionsupporting

confidence: 64%

“…1d). In sharp contrast to MCF-7 cells [27], viability of SUM159 cells was not affected by stable knockdown of Bmi-1 protein (Fig. 1c,d).…”

Section: Resultsmentioning

confidence: 80%

“…Even though the published literature on the role of Bmi-1 in regulation of apoptosis is ambiguous [27, 29], we were tempted to test if the proapoptotic response to BITC was affected by overexpression or knockdown of Bmi-1 protein. Figure 2a shows early (Annexin V high and propidium iodide low ) and late apoptotic fraction (Annexin V high and propidium iodide high ) in MCF-7 and SUM159 cells after 24 h treatment with DMSO or BITC.…”

Section: Resultsmentioning

confidence: 99%

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The role of polycomb group protein Bmi-1 and Notch4 in breast cancer stem cell inhibition by benzyl isothiocyanate

Kim

Singh

2015

Breast Cancer Res Treat

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We showed previously that garden cress constituent benzyl isothiocyanate (BITC) inhibits self-renewal of breast cancer stem cells (bCSC) in vitro and in vivo. The present study offers novel insights into the mechanism by which BITC inhibits bCSC. Flow cytometry and mammosphere assay was performed to quantify bCSC fraction. Protein expression was determined by western blotting. Apoptosis was assessed by flow cytometry using Annexin V-propidium iodide method. Cell migration was determined by Boyden chamber assay. BITC treatment resulted in a marked decrease in protein level of polycomb group protein B-lymphoma Moloney murine leukemia virus insertion region-1 (Bmi-1) in cultured human breast cancer cells (MCF-7, SUM159, MDAMB-231 and MDA-MB-361) and MDA-MB-231 xenografts in vivo. Overexpression (MCF-7) or knockdown (SUM159 and MDA-MB-231) of Bmi-1 protein had no meaningful impact on the BITC’s ability to inhibit cell viability and cell migration and/or induce apoptosis. On the other hand, inhibition of bCSC markers (aldehyde dehydrogenase 1 activity and mammosphere frequency) resulting from BITC exposure was significantly altered by Bmi-1 overexpression and knockdown. BITC was previously shown to cause activation of Notch1, Notch2 and Notch4 in association with induction of γ-secretase complex component Nicastrin, which are also implicated in maintenance of cancer stemness. BITC-mediated inhibition of bCSC was augmented by knockdown of Notch4 and Nicastrin, but not by RNA interference of Notch1 or Notch2. The present study highlights important roles for Bmi-1 and Notch4 in BITC-mediated suppression of bCSC.

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“…In agreement with published data [27], overexpression of Bmi-1 protein (Fig. 1c) led to a significant (1.6-fold) increase in MCF-7 cell viability (Fig.…”

Section: Resultssupporting

confidence: 93%

Section: Discussionsupporting

confidence: 64%

“…1d). In sharp contrast to MCF-7 cells [27], viability of SUM159 cells was not affected by stable knockdown of Bmi-1 protein (Fig. 1c,d).…”

Section: Resultsmentioning

confidence: 80%

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

The role of polycomb group protein Bmi-1 and Notch4 in breast cancer stem cell inhibition by benzyl isothiocyanate

Kim

Singh

2015

Breast Cancer Res Treat

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show abstract

“…Bmi-1 has been shown to be an upstream regulator of the PI3K/Akt pathway [13,18,19], which plays a critical role in regulation of the EMT process and cell migration. Our data shows that Bmi-1 knockdown is correlated to reduced phosphorylation of Akt after the IR treatment (Fig.…”

Section: Resultsmentioning

confidence: 99%

Role of Bmi-1 in Regulation of Ionizing Irradiation-Induced Epithelial-Mesenchymal Transition and Migration of Breast Cancer Cells

Yuan

Zhang

et al. 2015

PLoS ONE

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Radiotherapy is a widely used treatment for cancer. However, recent studies suggest that ionizing radiation (IR) can promote tumor invasion and metastasis. Bmi-1, a member of the polycomb group protein family, has been observed as a regulator of oxidative stress and promotes metastasis in some tumors. But, its potential role in the metastasis induced by IR of breast cancer has not been explored. In our study, we found that increased levels of Bmi-1 were correlated to EMT of breast cancer cells. Through analyzing the EMT state and metastasis of breast cancer induced by IR, we found the metastatic potential of breast cancer cells can either be inhibited or accelerated by IR following a time-dependent pattern. Silencing Bmi-1 completely abolished the ability of the IR to alter, reduce or increase, the migration of breast cancer cells. Also, when Bmi-1 was knocked down, the effect of inhibition of PI3K/AKT signaling on EMT affected by IR was blocked. These results suggest that Bmi-1 is a key gene in regulation of EMT and migration of breast cancer cells induced by IR through activation of PI3K/AKT signaling; therefore, Bmi-1 could be a new target for inhibiting metastasis caused by IR.

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Non‐coding RNA and cholesteatoma

Jovanović

Živković

Jesić

et al. 2022

Laryngoscope Investig Oto

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Objective: Cholesteatoma is a challenging chronic pathology of the middle ear for which pharmacologic therapies have not been developed yet. Cholesteatoma occurrence depends on the interplay between genetic and environmental factors while master regulators orchestrating disease progression are still unknown. Therefore, in this review, we will discuss the diagnostic and therapeutic potential of non-coding RNAs (ncRNA) as a new class of regulatory molecules. Methods:We have comprehensively reviewed all articles investigating ncRNAs, specifically micro RNAs (miRNAs) and long ncRNAs (lncRNA/circRNA) in cholesteatoma tissue.Results: Candidate miRNA approaches indicated that miR-21 and let-7a are the major miRNAs involved in cholesteatoma growth, migration, proliferation, bone destruction, and apoptosis. Regulatory potential for the same biological processes was also observed for miR-203a. The NF-kB/miR-802/PTEN regulatory network was in relation to observed miR-21 activity in cholesteatoma as well. High throughput approaches revealed additional ncRNAs implicated in cholesteatoma pathology. Competitive endogenous RNA (ceRNA) analysis highlighted lncRNA/circRNA that could be "endogenous sponge" for miR-21 and let-7a based on the hypothesis that RNA transcripts can communicate with and regulate each other by using shared miRNA response elements. Conclusion:In this review, we summarize the discoveries and role of ncRNA in major pathways in cholesteatoma and highlight the potential of miRNA-based therapeutics in the treatment of cholesteatoma.

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Knockdown of the Bmi-1 oncogene inhibits cell proliferation and induces cell apoptosis and is involved in the decrease of Akt phosphorylation in the human breast carcinoma cell line MCF-7

Cited by 19 publications

References 29 publications

The role of polycomb group protein Bmi-1 and Notch4 in breast cancer stem cell inhibition by benzyl isothiocyanate

The role of polycomb group protein Bmi-1 and Notch4 in breast cancer stem cell inhibition by benzyl isothiocyanate

Role of Bmi-1 in Regulation of Ionizing Irradiation-Induced Epithelial-Mesenchymal Transition and Migration of Breast Cancer Cells

Non‐coding RNA and cholesteatoma

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