It is verified that long non-coding RNAs (lncRNAs) play crucial roles in various cancers. LncRNA LEF1-AS1 is a reported oncogene in colorectal cancer and glioblastoma. In this study, we unveiled that LEF1-AS1 markedly increased in oral squamous cell carcinoma (OSCC) tissues and cell lines. Besides, OSCC patients with high levels of LEF1-AS1 were apt to poor prognosis. Functionally, LEF1-AS1 knockdown inhibited cell survival, proliferation and migration, whereas enhanced cell apoptosis and induced G0/G1 cell cycle arrest in vitro. Consistently, LEF1-AS1 silence hindered tumor growth in vivo. Moreover, LEF1-AS1 inhibition stimulated the activation of Hippo signaling pathway through directly interacting with LATS1. Furtherly, we disclosed that LEF1-AS1 silence abolished the interaction of LEF1-AS1 with LATS1 while enhanced the binding of LATS1 to MOB, therefore promoting YAP phosphorylation but impairing YAP1 nuclear translocation. Additionally, we demonstrated that LEF1-AS1 regulated YAP1 translocation via a LATS1-dependent manner. Furthermore, we also uncovered that YAP1 overexpression abolished the suppressive impact of LEF1-AS1 repression on the biological processes of OSCC cells. In a word, we concluded that LEF1-AS1 served an oncogenic part in OSCC through suppressing Hippo signaling pathway by interacting with LATS1, suggesting the therapeutic and prognostic potential of LEF1-AS1 in OSCC.
Objectives
It has been widely reported that long non‐coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA HLA complex group 11 (HCG11) has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of HCG11 in glioma.
Materials and methods
Based on The Cancer Genome Atlas (TCGA) data set and qRT‐PCR analysis, the expression pattern of HCG11 was identified in glioma samples. The mechanism associated with HCG11 downregulation was determined by mechanism experiments. Gain‐of‐function assays were conducted for the identification of HCG11 function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull‐down assay was used to explore the downstream molecular mechanism of HCG11. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.
Results
HCG11 was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of HCG11 efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. HCG11 was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging micro‐496 to upregulate cytoplasmic polyadenylation element binding protein 3 (CPEB3). CEPB3 and miR‐496 involved in HCG11‐mediated glioma progression.
Conclusions
HCG11 inhibited glioma progression by regulating miR‐496/CPEB3 axis.
Background: LncRNAs play crucial roles in the development of carcinomas. However, the investigation of LINC00662 in Oral squamous cell carcinoma (OSCC) is still elusive. Methods: qRT-PCR assay tested the expression levels of LINC00662, hnRNPC and AK4. With exposure to irradiation, CCK-8, colony formation, flow cytometry and western blot experiments, respectively determined the function of LINC00662 in the radiosensitivity of OSCC cells. Then RIP and western blot assays affirmed the interaction between hnRNPC protein and LINC00662 or AK4. Finally, rescue assays validated the regulation mechanism of LINC00662 in the radioresistance of OSCC. Results: In the present report, LINC00662 was overexpressed in OSCC and its silencing could alleviate radioresistance of OSCC. Furthermore, the interaction between hnRNPC protein and LINC00662 or AK4 was uncovered. Besides, LINC00662 regulated AK4 mRNA stability through binding to hnRNPC protein. To sum up, LINC00662 modulated the radiosensitivity of OSCC cells via hnRNPC-modulated AK4. Conclusion: The molecular mechanism of the LINC00662/hnRNPC/AK4 axis was elucidated in OSCC, which exhibited a promising therapeutic direction for patients with OSCC.
Thyroid carcinoma is the most widespread malignancy in endocrine system with the increasing incidence. Despite of the advanced approaches to the management of thyroid carcinoma, the therapeutic effects remain unpleasant largely due to the radiosensitivity of thyroid carcinoma cells. LncRNAs play important part in the tumorigenesis and development, especially in the radiosensitivity of tumor cells. However, their roles in thyroid carcinoma still needed to be explored deeply. The purpose of our research is to inspect the possible biological role and regulation mechanism of LINC00511 desirable for therapies of thyroid carcinoma patients. In the present study, LINC00511 was significantly overexpressed in thyroid carcinoma and its silencing boosted radiosensitivity of thyroid carcinoma cells. Then we unveiled that LINC00511 regulated JAK2/STAT3 signaling pathway which was resistant to radiation treatment. Besides, TAF1 modulated JAK2 at transcriptional level. Moreover, LINC00511 bound to TAF1 and further promoted JAK2 expression. In conclusion, rescue experiments verified that the radiosensitivity of thyroid carcinoma cells was attributed to LINC00511/TAF1/JAK2/STAT3 axis. The current paper investigated the underlying mechanism of LINC00511 and set a new therapeutic direction for the therapy of thyroid carcinoma.
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