Abstract
BackgroundBreast cancer is one the most common cancers, making it the second leading cause of cancer-related death among women. Long non-coding RNAs (lncRNAs), with tightly regulated expression patterns, also serve as tumor suppressor during tumorigenesis. The present study aimed to elucidate the role of LINC00968 in breast cancer via WNT2-mediated Wnt2/β-catenin signaling pathway.MethodsBreast cancer chip GSE26910 was utilized to identify differential expression in LINC00968 and WNT2. The possible relationship among LINC00968, transcriptional repressor HEY and WNT2 was analyzed and then verified. Effects of LINC00968 on activation of the Wnt2/β-catenin signaling pathway was also tested. Drug resistance, colony formation, cell migration, invasion ability and cell apoptosis after transfection were also determined. Furthermore, tumor xenograft in nude mice was performed to test tumor growth and weight in vivo.ResultsWNT2 expression exhibited at a high level, whereas LINC00968 at a low expression in breast cancer which was also associated with poor prognosis in patients. LINC00968 targeted and negatively regulated WNT2 potentially via HEY1. Either overexpressed LINC00968 or silenced inhibited activation of the Wnt2/β-catenin signaling pathway, thereby reducing drug resistance, decreasing colony formation ability, as well as suppressing migration and invasion abilities of breast cancer cells in addition to inducing apoptosis. Lastly, in vivo experiment suggested that LINC00968 overexpression also suppressed transplanted tumor growth in nude mice.ConclusionCollectively, overexpressed LINC00968 contributes to reduced drug resistance in breast cancer cells by inhibiting the activation of the Wnt2/β-catenin signaling pathway through silencing WNT2. This study offers a new target for the development of breast cancer treatment.
Highlights
Breast cancer is one the most common cancers, making it the second leading cause of cancer-related death among women
The results showed that LINC00968 expression was low while expression of WNT2 was high in breast cancer (Fig. 1A)
MEM website confirmed that LINC00968 and WNT2 exhibits co-expression with the latter playing a role in the Wnt2/β-catenin signaling pathway (Table 2)
Summary
Breast cancer is one the most common cancers, making it the second leading cause of cancer-related death among women. Long non-coding RNAs (lncRNAs), with tightly regulated expression patterns, serve as tumor suppressor during tumorigenesis. Breast cancer was regarded as the second leading cause of death caused by cancer among women after lung cancer [1]. Chemotherapy is the treatment of choice for breast cancer which initiates tumor. A series of lncRNAs have been demonstrated to be considered as tumor markers in breast cancer [10, 11]. Expressed lncRNA p10247 was reported to be closely correlated with reinforced growth and metastatic potential of breast cancer cells [12]. A recent study has found that LINC00968, a lncRNA, has a potential in the treatment of non-small cell lung cancer [14]. Our work using microarray demonstrated that low levels of LINC00968 was found in breast cancer
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