LINC00899 suppresses the progression of triple-negative breast cancer via the miRNA-425/PTEN axis and is a biomarker for neoadjuvant chemotherapy efficacy

PTEN公司 三阴性乳腺癌 医学 生物标志物 乳腺癌 癌症研究 小RNA 肿瘤科 癌症 内科学 基因 生物 PI3K/AKT/mTOR通路 细胞凋亡 遗传学
作者
Lianjie Niu,Yongtao Bai,Yu Meng,Xianfu Sun
出处
期刊:Journal of Cancer [Ivyspring International Publisher]
卷期号:16 (5): 1647-1655
标识
DOI:10.7150/jca.100619
摘要

Background: Close clinical attention has been paid to triple-negative breast cancer (TNBC) due to its poor prognosis, high recurrence and mortality rates and rapid invasion and metastasis. The present study aimed to explore the potential mechanism of LINC00899 in the progression of TNBC and its effect on the proliferation and migration of TNBC cells via the microRNA (miR)-425/phosphatase and tensin homolog (PTEN) axis. Methods: For this purpose, plasma exosomes and related clinical data from 119 patients with breast cancer receiving neoadjuvant chemotherapy (59 patients with TNBC, 32 with HER2+ and with 28 luminal-type) and 20 healthy women were collected. Functional assays were then used to verify the role of the LINC00899/miR-425/PTEN axis in the proliferation and migration of TNBC cells. Results: The results showed that the expression of LINC00899 was reduced in plasma exosomes and breast cancer cell lines, which was associated with the Ki-67 index, tumor size and the presence or absence of lymph node metastasis but was not associated with patient age, androgen receptor expression or cholangiocarcinoma thrombus. The receiver operating characteristic curve results showed that LINC00899 had a high predictive value for the pathological outcome of patients with TNBC receiving neoadjuvant treatment. The results of the functional experiments also showed that LINC00899 targeted and regulated miR-425 in TNBC, and miR-425 negatively regulated the expression of PTEN. Conclusions: In conclusion, the results of the present indicated that LINC00899 may predict neoadjuvant chemotherapy efficacy in patients with TNBC and that LINC00899 inhibited the proliferation and migration of MDA-MB-231 cells via the miR-425/PTEN axis.
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