Background: The long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression.
Methods: We used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial-mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an nude mouse model of tumorigenesis.
Results: We established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth .
Conclusions: Our study reveals that LINC00467 promotes prostate cancer progression M2 macrophage polarization and the miR-494-3p/STAT3 axis.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8170392 | PMC |
| http://dx.doi.org/10.3389/fonc.2021.661431 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
[High expression of LINC00467 promotes proliferation and metastasis of lung adenocarcinoma cells by suppressing autophagy inhibiting the AMPK/mTOR pathway].
Nan Fang Yi Ke Da Xue Xue Bao
October 2024
Department of Respiratory Medicine, First Affiliated Hospital of Wannan Medical College, Wuhu 241001, China.
Objective: To investigate the regulatory effects of LINC00467 on proliferation and metastasis of lung adenocarcinoma cells and the involvement of autophagy in its regulatory mechanism.
Methods: LINC00467 expression levels in lung adenocarcinoma tissues and their correlation with the patients' survival outcomes were analyzed using data from TCGA database. LINC00467 expression was also examined using qRT-PCR in human bronchial epithelial cells 16HBE and lung adenocarcinoma cell lines A549 and H1299.
Multi-omics integration analysis reveals the role of N6-methyladenosine in lncRNA translation during glioma stem cell differentiation.
Brief Funct Genomics
December 2024
Department of Biomedical Engineering, Nanjing University of Aeronautics and Astronautics, No. 29 Jiangjun Avenue, Jiangning District, Nanjing 211106, Jiangsu Province, China.
Article Synopsis
- Glioblastoma is a highly lethal brain cancer, and recent studies suggest that m6A modifications interact with long noncoding RNAs (lncRNAs), playing a role in tumor development and progression.* -
- This research analyzed the transcriptomes, translatomes, and epitranscriptomics of glioma stem and differentiated cells, revealing that lncRNAs with many m6A modifications have lower translation efficiency.* -
- The study found that m6A peaks located downstream of short open reading frames (sORFs) more strongly inhibit lncRNA translation, highlighting the complex regulatory role of m6A in glioblastoma.*
lncRNA Biomarkers of Glioblastoma Multiforme.
Biomedicines
April 2024
Department of Medical Genetics, Third Faculty of Medicine, Charles University, Ruská 87, Vinohrady, 10000 Prague, Czech Republic.
Long noncoding RNAs (lncRNAs) are RNA molecules of 200 nucleotides or more in length that are not translated into proteins. Their expression is tissue-specific, with the vast majority involved in the regulation of cellular processes and functions. Many human diseases, including cancer, have been shown to be associated with deregulated lncRNAs, rendering them potential therapeutic targets and biomarkers for differential diagnosis.
View Article and Find Full Text PDFLINC00467 enhanced the proliferative, migratory and invasive ability of breast cancer cells by targeting miR-18a/b-5p/MAPK4 axis.
Cell Mol Biol (Noisy-le-grand)
December 2023
Department of Galactophore, Fujian Maternity and Child Health Hospital, Fuzhou, 350001, Fujian Province, China.
Breast cancer (BC) is a common gynaecological malignancy worldwide. Long noncoding RNAs (lncRNAs) were identified to take part in the regulation of the occurrence and development of tumors. LncRNA The role of LINC00467 in lung adenocarcinoma has been reported, but its mechanism remains unclear in BC.
View Article and Find Full Text PDFLINC00467 mediates the 5-fluorouracil resistance in breast cancer cells.
In Vitro Cell Dev Biol Anim
January 2024
Department of Oncology, the Affiliated Hospital of Southwest Medical University, Taping Rd. No.25, Luzhou, China.
Breast cancer is a prevalent global disease that requires the development of effective therapeutic approaches. The occurrence of 5-fluorouracil (5-FU) resistance in breast cancer is emerging, which urgently needs new way to overcome the obstacle. In this study, we validated that the expression of LINC00467 is up-regulated in the breast cancer patients and breast cancer cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!