DESCRIPTION:

Genes that are downregulated directly or indirectly by Mir302b in MDA-MB-231 or BT-549 cells made cisplatin-sensitive by overexpression of Mir302b. HGNC identifiers were manually assigned. Therapy:Cisplatin. Response Type:Sensitive

LABEL:

DR in CP-sensitive TNBC

SCORE TYPE:

Binary

DATE ADDED:

2017-06-03

DATE UPDATED:

2020-05-06

SPECIES:

AUTHORS:

Cataldo A, Cheung DG, Balsari A, Tagliabue E, Coppola V, Iorio MV, Palmieri D, Croce CM

TITLE:

miR-302b enhances breast cancer cell sensitivity to cisplatin by regulating E2F1 and the cellular DNA damage response.

JOURNAL:

Oncotarget Jan 2016, Vol 7, pp. 786-97

ABSTRACT:

The identification of the molecular mechanisms involved in the establishment of the resistant phenotype represents a critical need for the development of new strategies to prevent or overcome cancer resistance to anti-neoplastic treatments.Breast cancer is the leading cause of cancer-related deaths in women, and resistance to chemotherapy negatively affects patient outcomes. Here, we investigated the potential role of miR-302b in the modulation of breast cancer cell resistance to cisplatin.miR-302b overexpression enhances sensitivity to cisplatin in breast cancer cell lines, reducing cell viability and proliferation in response to the treatment. We also identified E2F1, a master regulator of the G1/S transition, as a direct target gene of miR-302b. E2F1 transcriptionally activates ATM, the main cellular sensor of DNA damage. Through the negative regulation of E2F1, miR-302b indirectly affects ATM expression, abrogating cell-cycle progression upon cisplatin treatment. Moreover miR-302b, impairs the ability of breast cancer cells to repair damaged DNA, enhancing apoptosis activation following cisplatin treatment.These findings indicate that miR-302b plays a relevant role in breast cancer cell response to cisplatin through the modulation of the E2F1/ATM axis, representing a valid candidate as therapeutic tool to overcome chemotherapy resistance. PUBMED: 26623722
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