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S-adenosylmethionine in combination with decitabine shows enhanced anti-cancer effects in repressing breast cancer growth and metastasis. | LitMetric

AI Article Synopsis

  • Abnormal DNA methylation contributes to cancer by silencing tumor suppressor genes and activating cancer-promoting genes, making the DNA methylation system a potential target for cancer treatment.
  • This study tested a combination of S-adenosylmethionine (SAM) and decitabine in a breast cancer model and found that it significantly reduced tumor size and lung metastasis compared to control and single-agent treatments.
  • Findings indicate that this combination therapy lowers key cancer markers and modifies genes linked to cancer pathways, supporting future research on epigenetic therapies for breast cancer treatment.

Article Abstract

Abnormal DNA methylation orchestrates many of the cancer-related gene expression irregularities such as the inactivation of tumour suppressor genes through hypermethylation as well as activation of prometastatic genes through hypomethylation. The fact that DNA methylation abnormalities can be chemically reversed positions the DNA methylation machinery as an attractive target for anti-cancer drug development. However, although in vitro studies suggested that targeting concordantly hypo- and hypermethylation is of benefit in suppressing both oncogenic and prometastatic functions of breast cancer cells, this has never been tested in a therapeutic setting in vivo. In this context, we investigated the combined therapeutic effects of an approved nutraceutical agent S-adenosylmethionine (SAM) and FDA-approved hypomethylating agent decitabine using the MDA-MB-231 xenograft model of breast cancer and found a pronounced reduction in mammary tumour volume and lung metastasis compared to the animals in the control and monotherapy treatment arms. Immunohistochemical assessment of the primary breast tumours showed a significantly reduced expression of proliferation (Ki-67) and angiogenesis (CD31) markers following combination therapy as compared to the control group. Global transcriptome and methylome analyses have revealed that the combination therapy regulates genes from several key cancer-related pathways that are abnormally expressed in breast tumours. To our knowledge, this is the first preclinical study demonstrating the anti-cancer therapeutic potential of using a combination of methylating (SAM) and demethylating agent (decitabine) in vivo. Results from this study provide a molecularly founded rationale for clinically testing a combination of agents targeting the epigenome to reduce the morbidity and mortality from breast cancer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521255PMC
http://dx.doi.org/10.1111/jcmm.15642DOI Listing

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