Background/Aims: Novel long non-coding RNA Fer-1-like protein 4 (FER1L4) has been reported to play crucial regulatory roles in tumor progression. However, its clinical significance and biological role in osteosarcoma (OS) is completely unknown. The aim of the present study was to investigate the role of FER1L4 in OS progression and the underlying mechanism. Methods: We analyzed the expression levels of FER1L4 in tissues of OS patients and cell lines via quantitative RT-PCR (qRT-PCR). The effect of FER1L4 on cell proliferation, colony formation, migration and invasion was analyzed by cell counting kit-8 (CCK-8), colony formation, wound healing and transwell invasion assay, respectively. Novel targets of FER1L4 were selected through a bioinformatics soft and confirmed using a dual-luciferase reporter system and qRT-PCR. To detect the role of FER1L4 in vivo tumorigenesis, tumor xenografts were created. Results: We found that the expression of FER1L4 was significantly downregulated in OS tissues and cell lines; moreover, low expression of FER1L4 was associated with advanced tumor-nude-metastasis (TNM) stage, lymph node metastases, and poor overall survival. Functional assays showed that upregulation of FER1L4 significantly inhibited OS cell proliferation, colony formation, migration, and invasion in vitro, as well as suppressed tumor growth in vivo. Assays performed to determine the underlying mechanism, indicated that FER1L4 interacted directly with miR-18a-5p. Subsequently, we found that FER1L4 significantly increased PTEN expression, a known target of miR-18a-5p, in OS cells. Furthermore, PTEN was found to be down-regulated, and positively correlated with FER1L4 in OS tissues. Conclusion: These findings suggest that FER1L4, acting as a competing endogenous RNA (ceRNA) of miR-18a-5p, exerts its anti-cancer role by modulating the expression of PTEN. Thus, FER1L4 may be a novel target for the prevention and treatment of OS.
The long intergenic non‐protein coding RNA regulator of reprogramming (lncRNA‐ROR) has been reported to play crucial regulatory roles in the pathogenesis and progression of multiple cancers. However, whether ROR is associated with the initiation and development of osteosarcoma (OS) remains unclear. Here, we found that ROR expression level was significantly up‐regulated in OS tissue samples compared to adjacent normal tissues, and the elevated ROR was closely correlated with advanced tumour‐node‐metastasis (TNM) stage and lymph node metastasis and poor overall survival rate. Functional assays showed that ROR knockdown suppressed the OS cell proliferation, colony formation, migration and invasion in vitro, and retarded tumour growth in vivo. In addition, miR‐206 was verified to be a target miRNA of ROR using bioinformatics online program and luciferase report assay. miR‐206 inhibition partially rescued the inhibitory effects on OS cells induced by ROR knockdown. In conclusion, these results suggested that ROR function as an oncogene in OS by sponging miR‐206 and might be a potential therapeutic target for patients with OS.
Introduction: The research of tumor-infiltrating lymphocytes (TILs) has attracted much attention in clinical practice in recent years. We performed this meta-analysis to find the value of tumor-infiltrating lymphocytes after neoadjuvant chemotherapy in triple negative breast cancer.
# Co-first author: W.T., G.L., X.X. * Co-Correspondence: C.G. and W.G.J. Abstract Background: Circulating tumor cells (CTCs) display changes in epithelial-mesenchymal transition (EMT) markers and miRNAs regulate EMT in breast cancer cells. The association between EMT characteristics and miRNA expression in CTCs of metastatic breast cancer (MBC) patients and their clinical implications remain unknown. Methods: CTC-specific miRNAs were screened based on comparison of the miRNA profile between CTC and primary tumor. RT-PCR was used to quantity the expression levels of EMT makers and miRNA candidates. We enrolled 219 MBC patients with CTCs ≥ 5/7.5mL blood from 2 cohorts and CTCs were detected and enriched by CellSearch. Overall survival (OS) and radiological response were analyzed. CTCs were divided into epithelial- (E-CTCs) and mesenchymal-like CTC (M-CTCs) phenotypes based on a cut-off value derived from suspended breast cancer cells recovered from PBMCs. Results: MiR-106b displayed upregulation in CTCs, with a higher level in M-CTCs than E-CTCs. Patients with E-CTCs showed better OS than those with M-CTCs (HR 1.77, 95% CI 1.14-2.78, P =0.012). CTCs from chemo-resistant MBC patients exhibited higher miR-106b. CTC-specific miR-106b was negatively associated with therapy response and OS (HR 1.73, 95% CI 1.06-2.84, P = 0.029). Conclusions: CTC-specific miR-106b was associated with EMT phenotypes of CTCs and may predict prognosis in MBC patients. Citation Format: Tan W, Liang G, Xie X, Tan L, Sanders AJ, Liu Z, Ling Y, Zhong W, Jiang WG, Gong C. Expression of miR-106b in circulating tumor cells is associated with EMT and prognosis in metastatic breast cancer patients [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P6-09-07.
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