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Involvement of miR-3648 mediated APC2 1 dysregulation in early onset and breast cancer progression

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Multiple cancers arise due to aberrations in the Wnt signaling pathway. Several miRNAs modulate the integral components of the wingless integrated (Wnt) signaling pathway. miR-3648 is a human-specific miRNAs that is of particular interest due to its minimal off-targeting effect. In this study, we investigated the expression of miR-3648 and APC2 in breast cancer patients of Pakistan. Correlations of miR-3648 and APC2 expression with clinico-pathological features and breast cancer subtypes were observed in tissue samples by means of quantitative real time PCR. Our results showed that miR-3648 was relatively downregulated in Luminal A subtype, with corresponding upregulation of APC2 in these patients. Moreover, the transcript levels of both miR-3648 and APC2 were found to be inversely regulated in breast cancer women presented with early disease onset, pre-menopause, low tumor grade, early clinical stage, absence of nodal invasion and metastasis, further suggesting the molecular interplay of these molecules in breast cancer development and progression.
Title: Involvement of miR-3648 mediated APC2 1 dysregulation in early onset and breast cancer progression
Description:
Multiple cancers arise due to aberrations in the Wnt signaling pathway.
Several miRNAs modulate the integral components of the wingless integrated (Wnt) signaling pathway.
miR-3648 is a human-specific miRNAs that is of particular interest due to its minimal off-targeting effect.
In this study, we investigated the expression of miR-3648 and APC2 in breast cancer patients of Pakistan.
Correlations of miR-3648 and APC2 expression with clinico-pathological features and breast cancer subtypes were observed in tissue samples by means of quantitative real time PCR.
Our results showed that miR-3648 was relatively downregulated in Luminal A subtype, with corresponding upregulation of APC2 in these patients.
Moreover, the transcript levels of both miR-3648 and APC2 were found to be inversely regulated in breast cancer women presented with early disease onset, pre-menopause, low tumor grade, early clinical stage, absence of nodal invasion and metastasis, further suggesting the molecular interplay of these molecules in breast cancer development and progression.

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