Abstract
Triple-negative breast cancer (TNBC) is a subtype of aggressive breast cancer with high recurrence and poor survival. Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play pivotal roles in the development and progression of multiple cancers. Although there are substantial studies revealing that lung cancer-associated transcript 1 (LUCAT1) functions as a tumor promotor in various human cancers, the molecular mechanism of LUCAT1 in TNBC remains largely to be explored. In our study, we identified that LUCAT1 expression was dramatically enhanced in TNBC samples and cells. High LUCAT1 expression was strongly associated with advanced stages and poor prognosis of TNBC. LUCAT1 contributed to TNBC development through accelerating cell proliferation, cell cycle progression and metastasis as well as attenuating cell apoptosis. Moreover, miR-5702 was proved to directly bind to LUCAT1 and be negatively modulated by LUCAT1. Knockdown of miR-5702 reversed the suppressing influences of LUCAT1 depletion on TNBC progression. In conclusion, it was the first investigation to shed light on the significant function and underlying regulatory mechanism of LUCAT1 in TNBC tumorigenesis. We validated that LUCAT1 induced tumorigenesis and metastasis of TNBC via miR-5702, which provided clues for improving the treatment of TNBC.
Highlights
Breast cancer remains the most prevalent diagnosed malignant neoplasm and ranks the first leading cause of cancer-related death among women worldwide [1,2]
In order to probe the biological role of lung cancer-associated transcript 1 (LUCAT1) in Triple-negative breast cancer (TNBC) progression, we measured the expression of LUCAT1 in 94 recruited TNBC specimens and corresponding adjacent specimens
Our investigation exhibited that LUCAT1 expression was prominently increased in TNBC tissues compared to matched non-tumor tissues (Figure 1A)
Summary
Breast cancer remains the most prevalent diagnosed malignant neoplasm and ranks the first leading cause of cancer-related death among women worldwide [1,2]. It is well known that breast cancer is a heterogeneous disease whose gene-expression profiles are various between individuals [3]. TNBC is characterized by absence of estrogen receptor (ER), progesterone receptor (PR) along with human epidermal growth factor receptor-2 (HER2) [6]. It has been reported ER, PR, and HER2 are of immense importance in the clinical diagnosis and therapy for breast cancer [7]. For lacking ER, PR, and HER2 expression, there are only a few effective adjuvant treatments of patients with TNBC, including conventional surgery, radiotherapy, and chemotherapy [8]. It is of great clinical significance to develop reliable molecular therapeutic targets for TNBC patients
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