Hair follicle stem cell proliferation and differentiation are achieved by miR-1285-3P through targeted regulation of NOTCH pathway.

The purpose of this experiment is to understand how miR-1285-3P regulates the NOTCH signaling pathway by targeting, thereby affecting the proliferation and differentiation of hair follicle stem cells. The cultured Inner Mongolia hair follicle stem cells were used in this experiment, and they were divided into control group, blank transfection group and miR-1285-3P transfection group. Among them, the control group was left untreated; the blank group was given miR-NC transfection; at the same time, the miR-1285-3P transfection group was given miR-1285-3P mimics for transfection. Compared with the control group (97.24 ± 6.81) and blank gro transfection up (97.32 ± 7.20), the cell proliferation ability of the miR-1285-3P transfection group (49.31 ± 3.39) was significantly lower. Compared with the other two groups, The proliferation ability of cells in the miR-1285-3P transfection group was decreased (P < 0.05); compared with the S-phase hair follicle stem cells in the control group (19.23 ± 1.29) and blank transfection group (19.38 ± 1.45), the miR-1285-3P transfection group (15.26 ± 1.26) decreased more significantly (P < 0.05). For hair follicle stem cells in each group, the proportion of cells in the G0-G1 phase was significantly different between the blank transfection group (63.18 ± 2.78) and the control group (64.29 ± 2.09), and the blank transfection group had a higher proportion (P < 0.05). In the process of miR-1285-3P targeting and regulating NOTCH signaling pathway, the proliferation and differentiation ability of hair follicle stem cells is affected. When NOTCH signaling pathway is activated, the differentiation of hair follicle stem cells is accelerated.

LncRNA TCTN2 Promotes the Malignant Development of Hepatocellular Carcinoma via Regulating mIR-1285-3p/ARF6 Axis.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most life-threatening malignant diseases. TCTN2 protein participates in tumorigenesis and development. However, whether lncRNA TCTN2 is associated with HCC pathogenesis remains unclear. METHODS: The expression of lncRNA, TCTN2, miR-1285-3p, and ARF6 in HCC tissues and cells was detected by a quantitative Real-Time PCR (qRT-PCR) assay. lncRNA TCTN2-specific shRNA was transfected into HCC cells, and a functional investigation was performed. The direct interactions between lncRNA TCTN2 and miR-1285-3p and ARF6 were verified by dualluciferase reporter gene assay. A rescue experiment was performed to confirm the role of miR- 1285-3p/ARF6 in association with lncRNA TCTN2. RESULTS: LncRNA TCTN2 exhibited a high expression in HCC tumor tissues and cell lines. Knockdown of lncRNA TCTN2 suppressed cell proliferation and induced cell cycle arrest and apoptosis through regulating Cyclin D1/p21 and Bax/Bcl-2 signals. Meanwhile, the knockdown of lncRNA TCTN2 inhibited HCC cell migration and invasion through upregulating MMP2/MMP9. Mechanistic investigation revealed that lncRNA TCTN2 upregulated the expression of ARF6 via sponging miR-1285-3p. Rescue experiments indicated that miR-1285-3p inhibitor reversed the antitumor effects of lncRNA TCTN2 and ARF6 knockdown inhibited the progression of HCC. CONCLUSION: Our results suggested that the knockdown of lncRNA TCTN2 inhibited HCC development by regulating the miR-1285-3p/ARF6 axis, implying that the lncRNA TCTN2 is upregulated in HCC and may serve as a diagnostic biomarker in HCC. Furthermore, it may demonstrate an important value for the clinical treatment of patients with HCC.

CircRNA_400029 promotes the aggressive behaviors of cervical cancer by regulation of miR-1285-3p/TLN1 axis.

Background: Cervical cancer (CC) is the highest incidence of female malignant tumor in China. Circular RNAs (circRNAs) has been reported to affect CC progression by altering mRNA stability at the transcriptional level or binding to miRNAs to produce competitive endogenous RNA (ceRNA). For this purpose, our study was aimed to investigate the function effects and the potential regulatory mechanism of the circRNA_400029 in CC cells. Materials and methods: The expression levels of circRNA_400029 and miR-1285-3p were detected by real time polymerase chain reaction (RT-PCR). Similarly, the mRNA and protein levels of TLN1 (Talin 1) was detected by RT-PCR and Western blot. Cell-Counting Kit-8 (CCK-8), EdU and Flow cytometry assay were used to detect cell proliferation, cell cycle and apoptosis. Then the Transwell assays were used to test cell migration and invasion. Besides this, the functional targets were confirmed by Dual luciferase reporter assays. Tumor xenograft in nude mice checked the result in vivo. Results: To begin with, circRNA_400029 was upregulated in CC cells and tissue. Knockdown circRNA_400029 inhibited cell proliferation, migration and invasion while induced cell apoptosis. Interestingly, miR-1285-3p targeted circRNA_400029 and down-regulated of miR-1285-3p could reverse the effects of circRNA_400029 weak-expression on progression and apoptosis of CC cells. Moreover, TLN1 was up-regulated in CC cells and identified as a direct target of miR-1285-3p. Meanwhile, we found that miR-1285-3p negatively regulated the function of TLN1. Finally, the circRNA_400029/miR-1285-3p/TLN1 axis could affect tumor growth in vivo. Conclusion: The overexpressed circRNA_400029 promoted CC proliferation, migration and invasion while deduced apoptosis by sponging miR-1285-3p to regulate TLN1. CircRNA_400029 was a potential onco-circRNA in CC, and might be a promised therapy target.

Linc00467 promotes invasion and inhibits apoptosis of head and neck squamous cell carcinoma by regulating miR-1285-3p/TFAP2A.

OBJECTIVE: To explore the invasion and apoptosis of head and neck squamous cell carcinoma (HNSCC) regulated by Linc00467 through the miR-1285-3p/TFAP2A axis. METHODS: qRT-PCR was used to detect the expressions of Linc00467, miR-1285-3p, and TFAP2A in tissues and cells of HNSCC patients. The targeting relationships between Linc00467 and miR-1285-3p, miR-1285-3p, and TFAP2A were verified by dual-luciferase reporter assay. Transfection and grouping were carried out, after HNSCC cell lines were screened. Transwell assay and flow cytometry were used to test cell invasion and apoptosis, respectively. RESULTS: Compared with normal tissues adjacent to the tumor, the expressions of Linc00467 and TFAP2A increased significantly in cancer tissues, while the expression of miR-1285-3p decreased (all P<0.05). Compared with the si-NC group, the invasion of the si-Linc00467 group decreased and the apoptosis rate increased (both P<0.05). In HNSCC cells, over-expression of Linc00467 promoted increased cell invasion and decreased apoptosis rate, which could be partially rescued by over-expression of miR-1285-3p (all P<0.05). Over-expression of miR-1285-3p caused decreased cell invasion and increased apoptosis rate, which was partially reversed by over-expression of TFAP2A (all P<0.05). CONCLUSION: Linc00467 can be used as ceRNA to adsorb miR-1285-3p to regulate the expression of TFAP2A, promote invasion and inhibit apoptosis of HNSCC cells. Linc00467 inhibitors may become one of the targeted therapeutic drugs for HNSCC.

LncRNA LEF1-AS1 Promotes Ovarian Cancer Development Through Interacting with miR-1285-3p.

BACKGROUND: Growing evidence indicates that long noncoding RNA (lncRNA) is a group of important regulator in cancer development. However, the correlation between lncRNA and ovarian cancer remains elusive. Here, we aimed to investigate the roles of LEF1-AS1 in ovarian cancer progression. METHODS: LEF1-AS1 expression was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Survival rate was analyzed by Kaplan-Meier method. Cell Counting Kit-8 (CCK8) and colony formation assays were used for proliferation analysis. Transwell assay was utilized for analyses of migration and invasion. Luciferase reporter assay was performed to test the interaction between LEF1-AS1 and miR-1285-3p. RESULTS: We showed that LEF1-AS1 expression was upregulated in ovarian cancer tissues compared with normal tissues. Besides, LEF1-AS1 level was positively correlated with lymph node metastasis and advanced stage. Enhanced expression of LEF1-AS1 may predict a poor prognosis. Moreover, LEF1-AS1 knockdown suppressed ovarian cancer cell proliferation, migration and invasion. Mechanistically, LEF1-AS1 exerted its oncogenic functions through interacting with miR-1285-3p to inhibit miRNA activity. Rescue assay validated that miR-1285-3p inhibitors abrogated LEF1-AS1-silencer-caused suppression of ovarian cancer progression. CONCLUSION: Our study revealed that LEF1-AS1 acts as a vital regulation in ovarian cancer progression.

Long non-coding RNA RBM5-AS1 promotes the aggressive behaviors of oral squamous cell carcinoma by regulation of miR-1285-3p/YAP1 axis.

The human genome encodes far more long non-coding RNA (lncRNA) genes than protein coding genes. However, the function of majority of the lncRNAs is poorly understood. Numerous lncRNAs were aberrantly expressed in various cancers and found to be associated with development and progression of cancer. Little is known about the role of lncRNAs in oral squamous cell carcinoma (OSCC). In this study, we identified lncRNA RBM5-AS1 to be highly expressed in OSCC tumor tissues and cancer cell lines. RBM5-AS1 promotes the proliferation, migration, and invasion of OSCC cells in vitro. We also found that RBM5-AS1 regulates the level of miR-1285-3p as a competitive endogenous RNA (ceRNA), therefore regulate the expression level of an oncogene-YAP1, a target of miR-1285-3p. The information obtained in this study is valuable for understanding the regulatory mechanism of lncRNA in the development of OSCC and for developing new strategies for the diagnosis and treatment of OSCC.

TNF-α-induced lncRNA LOC105374902 promotes the malignant behavior of cervical cancer cells by acting as a sponge of miR-1285-3p.

Long noncoding RNAs (lncRNAs) regulate gene expression at epigenetic, transcriptional, post-transcriptional levels and play important roles in tumorigenesis and inflammation. In order to explore the effects of lncRNAs on the malignant behavior of cervical cancer (CC) which may be involved in mechanism stimulated by inflammatory factors, we screened a differential expression profile of lncRNAs in CC cells stimulated by TNF-α by deep sequencing. We characterized a significantly upregulated lncRNA LOC105374902 induced by TNF-α. Then, we found that TNF-α accelerated the binding of STAT3 to the promoter region of lncRNA LOC105374902 and promoted its expression. Mechanistically, lncRNA LOC105374902 directly bond to miR-1285-3p as a competing endogenous RNA (ceRNA) to derepress RPL14; functional analysis indicated that both lncRNA LOC105374902 and RPL14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) of CC cells. Taken together, TNF-α-induced lncRNA LOC105374902 may function as a ceRNA for miR-1285-3p to promote the expression of RPL14, promoting the migration, invasion and EMT of CC cells. These findings may provide new insights into the molecular pathogenesis of CC.

miR-1285-3p is a potential prognostic marker in human osteosarcoma and functions as a tumor suppressor by targeting YAP1.

BACKGROUND: Despite the major advances in the treatment, the overall survival of osteosarcoma remains poor. MicroRNAs (miRNAs) are involved in tumorigenesis and progression though modulating their target genes. In the present study, the roles of miR-1285-3p in osteosarcoma was investigated. METHODS: Microarray profiling was applied to distinguish the up and down regulated microRNAs in osteosarcoma. Quantitative real-time PCR (qRT-PCR) assay was performed to detect the expression of miR-1285-3p and YAP1 expression. MTT and transwell assays were carried out to determine the cells proliferation and invasion respectively. Moreover, dual luciferase reporter assay was performed to evaluate the binding efficiency between miR-1285-3p and the 3'UTR of YAP1. RESULTS: MiR-1285-3p was down regulated in osteosarcoma tissues and cell lines and the reduction of miR-1285-3p expression predicted a poor overall survival of osteosarcoma patients. Ectopic expression of miR-1285-3p inhibited osteosarcoma cell proliferation, colony formation and invasion. In addition, YAP1 was further demonstrated as a direct target of miR-1285-3p. Moreover, overexpression of YAP1 reversed the inhibitory effects of miR-1285-3p on osteosarcoma cells proliferation and invasion. CONCLUSIONS: MiR-1285-3p which was low expressed in osteosarcoma inhibited the proliferation and invasion of osteosarcoma cells via direct targeting YAP1. These results suggested that miR-1285-3p might be a potential therapeutic targets and biomarker in osteosarcoma.