BMI1 and PTEN are key determinants of breast cancer therapy: A plausible therapeutic target in breast cancer

Ramaiah, M. Janaki; Vaishnave, S

doi:10.1016/j.gene.2018.08.022

Cited by 39 publications

(30 citation statements)

References 95 publications

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“…BMI1 is an important epigenetic regulator and stem cell marker (7,10). Previous studies have demonstrated that inhibition of BMI1 can regulate the expression of MDR1, affect platinum transport and hydration, and promote the chemotherapy sensitivity of ovarian, breast and pancreatic cancer (40–42). As a homologue of BMI1, the function of Mel18, and the interaction of BMI1 and Mel18 have been widely studied.…”

Section: Discussionmentioning

confidence: 99%

Co‑inhibition of BMI1 and Mel18 enhances chemosensitivity of esophageal squamous cell carcinoma in�vitro and in�vivo

Wang

Zhu

et al. 2019

Oncol Lett

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Esophageal squamous cell carcinoma (ESCC) accounts for almost 90% of esophageal cancer cases and is the sixth most common cause of cancer-associated mortality worldwide. Cisplatin is the standard therapeutic reagent for ESCC; however, chemoresistance frequently occurs after a few weeks, which leads to ESCC recurrence. Aberrant expression of B lymphoma Mo-MLV insertion region 1 homolog (BMI1) has been reported to activate multiple growth-regulatory pathways, induce antiapoptotic abilities in numerous types of cancer cells and promote chemoresistance. However, to the best of our knowledge, the role of BMI1 in cisplatin-resistant ESCC, and the interaction between BMI1 and its homologue melanoma nuclear protein 18 (Mel18) remain unknown. The present study identified that knockdown of BMI1 promoted cytotoxic effects of cisplatin, and co-inhibition of Mel18 and BMI1 enhanced cisplatin-induced apoptosis and cytotoxicity. Inhibition of BMI1 and Mel18 also suppressed the expression of c-Myc. Furthermore, this combined inhibition sensitized esophageal xenograft tumors to cisplatin to a greater extent compared with BMI1 inhibition alone. In summary, the current study demonstrated that inhibition of BMI1 and Mel18 could increase the sensitivity of esophageal cancer cells to cisplatin via inhibition of c-Myc. Therefore, combined targeting of BMI1 and Mel18 may serve as a promising therapeutic strategy for sensitizing ESCC to chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Co‑inhibition of BMI1 and Mel18 enhances chemosensitivity of esophageal squamous cell carcinoma in�vitro and in�vivo

Wang

Zhu

et al. 2019

Oncol Lett

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“…Therefore, the overexpression of histone phosphorylation in cancer cells was regarded as a biomarker of cancer in recent years (Duong et al, 2010). In contrast, the ubiquitination of histones H2A and H2B in breast cancer cells mainly plays an important role in gene transcription and maintaining genome integrity (Cole et al, 2015;Janaki Ramaiah and Vaishnave, 2018). For instance, BMI-1 (Blymphoma Mo-MLV insertion region 1)which is a key player in the ubiquitination of histone H2A, was found to be correlated with advanced stages of breast cancer.…”

Section: Insight Into Other Histone Modificationsmentioning

confidence: 99%

Perspectives on the Role of Histone Modification in Breast Cancer Progression and the Advanced Technological Tools to Study Epigenetic Determinants of Metastasis

et al. 2020

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Metastasis is a complex process that involved in various genetic and epigenetic alterations during the progression of breast cancer. Recent evidences have indicated that the mutation in the genome sequence may not be the key factor for increasing metastatic potential. Epigenetic changes were revealed to be important for metastatic phenotypes transition with the development in understanding the epigenetic basis of breast cancer. Herein, we aim to present the potential epigenetic drivers that induce dysregulation of genes related to breast tumor growth and metastasis, with a particular focus on histone modification including histone acetylation and methylation. The pervasive role of major histone modification enzymes in cancer metastasis such as histone acetyltransferases (HAT), histone deacetylases (HDACs), DNA methyltransferases (DNMTs), and so on are demonstrated and further discussed. In addition, we summarize the recent advances of next-generation sequencing technologies and microfluidic-based devices for enhancing the study of epigenomic landscapes of breast cancer. This feature also introduces several important biotechnologists for identifying robust epigenetic biomarkers and enabling the translation of epigenetic analyses to the clinic. In summary, a comprehensive understanding of epigenetic determinants in metastasis will offer new insights of breast cancer progression and can be achieved in the near future with the development of innovative epigenomic mapping tools.

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“…Phosphatase and tensin homologue (PTEN) is a well-characterized tumor suppressor in breast cancer [39]. In one of the earlier studies describing an effect of resveratrol on promoter DNA methylation, it was reported that resveratrol was highly efficient in reducing PTEN promoter DNA methylation in MCF7 breast cancer cells [40].…”

Section: Methylationmentioning

confidence: 99%

Differential Methylation and Acetylation as the Epigenetic Basis of Resveratrol’s Anticancer Activity

et al. 2019

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Numerous studies support the potent anticancer activity of resveratrol and its regulation of key oncogenic signaling pathways. Additionally, the activation of sirtuin 1, a deacetylase, by resveratrol has been known for many years, making resveratrol perhaps one of the earliest nutraceuticals with associated epigenetic activity. Such epigenetic regulation by resveratrol, and the mechanism thereof, has attracted much attention in the past decade. Focusing on methylation and acetylation, the two classical epigenetic regulations, we showcase the potential of resveratrol as an effective anticancer agent by virtue of its ability to induce differential epigenetic changes. We discuss the de-repression of tumor suppressors such as BRCA-1, nuclear factor erythroid 2-related factor 2 (NRF2) and Ras Associated Domain family-1α (RASSF-1α) by methylation, PAX1 by acetylation and the phosphatase and tensin homologue (PTEN) by both methylation and acetylation, in addition to the epigenetic regulation of oncogenic NF-κB and STAT3 signaling by resveratrol. Further, we evaluate the literature supporting the potentiation of HDAC inhibitors and the inhibition of DNMTs by resveratrol in different human cancers. This discussion underlines a robust epigenetic activity of resveratrol that warrants further evaluation, particularly in clinical settings.

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BMI1 and PTEN are key determinants of breast cancer therapy: A plausible therapeutic target in breast cancer

Cited by 39 publications

References 95 publications

Co‑inhibition of BMI1 and Mel18 enhances chemosensitivity of esophageal squamous cell carcinoma in�vitro and in�vivo

Co‑inhibition of BMI1 and Mel18 enhances chemosensitivity of esophageal squamous cell carcinoma in�vitro and in�vivo

Perspectives on the Role of Histone Modification in Breast Cancer Progression and the Advanced Technological Tools to Study Epigenetic Determinants of Metastasis

Differential Methylation and Acetylation as the Epigenetic Basis of Resveratrol’s Anticancer Activity

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