Abstract
Mounting evidence suggests that long noncoding RNAs serve as specific biomarkers and potent modulators of multiple cancers. Long intergenic non-protein coding RNA 324 (LINC00324) is ubiquitously expressed in various tissues, including breast cancer. The biological function of LINC00324 in the development and progression of breast cancer remains unknown. Here, we fully elucidate the relation between LINC00324 expression and breast cancer, and suggest a potential mechanism of action. We found that decreased expression of LINC00324 was dramatically correlated with malignancy of breast cancer, both in breast cancer tissues and in cell lines. Overexpression of LINC00324 in MDA-MB-231 cells resulted in a decrease in cell proliferation, invasion, and migration, while increasing cells apoptosis. On the other hand, loss-of-function experiments indicated that deficiency of LINC00324 promoted malignant phenotypes in breast cancer cells. Mechanically, we found that LINC00324 is mainly distributed in the cytoplasm, fostering the expression of E-cadherin by sponging miR-10b-5p. Taken together, these findings suggest that LINC00324 plays a critical role in breast cancer progression by directly interacting with miR-10b-5p. LINC00324 can thus potentially act as an early diagnostic marker and a novel therapeutic agent for breast cancer.
Highlights
Breast cancer remains the most common cause of cancerrelated death in female patients, mortality rates have decreased in most developed countries
The results showed a decreased expression of LINC00324 in breast cancer tissues compared with adjacent normal tissues (Figure 1A)
We further investigated the relationship between LINC00324 expression and clinicopathologic features of breast cancer
Summary
Breast cancer remains the most common cause of cancerrelated death in female patients, mortality rates have decreased in most developed countries. Morbidity of breast cancer has surpassed uterine cancer, leapping to the top of female malignant tumors list in some cities of China [1]. According to distinct gene expression, breast cancer can be divided into at least five subtypes, including Luminal A, Luminal B, HER-2+, normal-like, and basal-like breast cancer [2, 3]. Powerful clinical treatment modalities for breast cancer, including chemoradiotherapy and surgical resection, have greatly improved over the past decade. The overall recurrence and metastasis rates remain high. Elucidating the molecular mechanism of and devising efficient treatment strategies for breast cancer are highly desirable
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