Abstract
The noncoding RNA termed urothelial carcinoma-associated 1 (UCA1) is an oncogenic lncRNA involved in promoting the growth of several tumors through various pathways. The aim of this study was to explore the expression of UCA1 in hypoxic breast cancer and its impact on tumorigenesis in low levels of oxygen. Here, we show that UCA1 is upregulated in a number of hypoxic (1% O2) breast cancer cells. In addition, UCA1 expression is significantly overexpressed in breast cancer tissues compared to matched normal cells. UCA1 knockdown in hypoxia inhibits breast cancer proliferation and induces apoptosis. The knockdown of hypoxia-inducible transcription factor 1α (HIF-1α) but not HIF-2α significantly decreases the expression of UCA1 in hypoxia. Overall, these findings indicate that UCA1 is a hallmark of hypoxic breast cancer and its expression is positively regulated by HIF-1α.
Highlights
Breast cancer is considered to be one of the most common solid tumors to involve a hypoxic tumor microenvironment and resist treatment [1,2,3]
Activation of hypoxia-inducible transcription factor (HIF-1) is used by cancer cells to adapt to the hypoxic microenvironment through regulating the expression of several genes involved in various biological process, such as cell proliferation, apoptosis, and tumor metastasis [11,12,13]
We show that urothelial carcinoma-associated 1 (UCA1) is commonly upregulated in hypoxic breast cancer cells and its overexpression is associated with tumor growth and inhibition of apoptosis in an HIF-dependent manner
Summary
Breast cancer is considered to be one of the most common solid tumors to involve a hypoxic tumor microenvironment and resist treatment [1,2,3]. E hypoxic tumor microenvironment is considered to be one of the important factors in overcoming treatment of solid tumors, including breast cancer [1, 8,9,10]. Activation of hypoxia-inducible transcription factor (HIF-1) is used by cancer cells to adapt to the hypoxic microenvironment through regulating the expression of several genes involved in various biological process, such as cell proliferation, apoptosis, and tumor metastasis [11,12,13]. Considering the fact that the majority of breast cancer cell deaths can be attributed to metastasis [28], understanding the key regulators involved in the promotion of breast cancer metastasis under stress conditions will be helpful in finding new targets for this cancer
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