TRIM29 inhibits miR-873-5P biogenesis via CYTOR to upregulate fibronectin 1 and promotes invasion of papillary thyroid cancer cells

Wu, Tong; Zhang, Dalin; Wang, Jiamei; Jiang, Jingyi; Du, Xin; Zeng, Xiaoyan; Du, Zhenhong

doi:10.1038/s41419-020-03018-3

Cited by 21 publications

(11 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the FN1 gene was found to be a key regulator in PTC development. Tripartite motif protein 29(TRIM29) promote the invasion and metastasis of PTC cells by up-regulating the expression of FN1 [23]. Furthermore, studies indicate that TGM2 activated FN1 through NF-κb to promote the invasion as well as metastasis of PTC [24].…”

Section: Discussionmentioning

confidence: 99%

Label-Free Proteome Profiling for Lymphatic Metastasis in Papillary Thyroid Carcinoma

Chen

Jiang

et al. 2022

Preprint

View full text Add to dashboard Cite

As the most common malignant tumor, the incidence of papillary thyroid carcinoma (PTC) has been significantly increased over the past few years. Approximately 30%-90% of patients with PTC present with cervical lymph node metastasis (LNM) at the time of initial diagnosis or follow-up, which has a serious impact on survival and prognosis. Six PTC N0 samples and six PTC N1b samples were collected. Proteins from the samples were analyzed by label-free quantitative proteomics. The bioinformatics of differentially expressed proteins (DEPs) was annotated with bioinformatic tools. The protein expression levels of the hub genes were verified using the HPA databases. Finally, we used the GEPIA database to perform survival analysis for the hub genes. A total of 1407 proteins were quantified under highly stringent criteria with fold change ≥ 2.0 and P < 0.05, and 95 DEPs were significantly changed between groups. Identified from the Cytoscape, the top 10 hub genes included FN1、CFL1、LGALS3、ANXA1、TIMP1、TPI1、MAPK1、HSPA9、ACTR2 and S100A11. We determined the hub genes expression in thyroid normal and cancer tissues using the HPA database. The expression of FN1 and ANXA1were closely related to disease free survival (DFS) and overall survival (OS) prognosis in PTC patients based on GEPIA database. These results revealed the pathways and mechanisms of LNM in PTC, thus providing a new perspective for the study of PTC with LNM. Together, these hub genes may have some clinical value in diagnosing PTC patients with LNM.

show abstract

Section: Discussionmentioning

confidence: 99%

Label-Free Proteome Profiling for Lymphatic Metastasis in Papillary Thyroid Carcinoma

Chen

Jiang

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…The contributions of lncRNAs to miRNAs biogenesis are gradually being revealed. Wu et al (2020) reported that lncRNA CYTOR represses miR-873-5p biogenesis via repressing the recruitment of DICER and TRBP to pre-miR-873 and further the cleavage of pre-miR-873. Zhang et al (2021) reported that lncRNA HOTAIRM1 represses miR-144 biogenesis via reducing pre-miR-144 stability and blocking the processing of pri-miR-144 by DROSHA.…”

Section: Discussionmentioning

confidence: 99%

SPINT1-AS1 Drives Cervical Cancer Progression via Repressing miR-214 Biogenesis

Song

Liu

Liang

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Accumulating evidences have revealed the dysregulated expressions and critical roles of non-coding RNAs in various malignancies, including cervical cancer. Nevertheless, our knowledge about the vast majority of non-coding RNAs is still lacking. Here we identified long non-coding RNA (lncRNA) SPINT1-AS1 as a novel cervical cancer-associated lncRNA. SPINT1-AS1 was increased in cervical cancer and correlated with advanced stage and poor prognosis. SPINT1-AS1 was a direct downstream target of miR-214, a well-known tumor suppressive microRNA (miRNA) in cervical cancer. Intriguingly, SPINT1-AS1 was also found to repress miR-214 biogenesis via binding DNM3OS, the primary transcript of miR-214. The interaction between SPINT1-AS1 and DNM3OS repressed the binding of DROSHA and DGCR8 to DNM3OS, blocked DNM3OS cleavage, and therefore repressed mature miR-214 biogenesis. The expression of SPINT1-AS1 was significantly negatively correlated with miR-214 in cervical cancer tissues, supporting the reciprocal repression between SPINT1-AS1 and miR-214 in vivo. Through downregulating mature miR-214 level, SPINT1-AS1 upregulated the expression of β-catenin, a target of miR-214. Thus, SPINT1-AS1 further activated Wnt/β-catenin signaling in cervical cancer. Functionally, SPINT1-AS1 drove cervical cancer cellular proliferation, migration, and invasion in vitro, and also tumorigenesis in vivo. Deletion of the region mediating the interaction between SPINT1-AS1 and DNM3OS, overexpression of miR-214, and inhibition of Wnt/β-catenin signaling all reversed the roles of SPINT1-AS1 in cervical cancer. Collectively, these findings identified SPINT1-AS1 as a novel cervical cancer-associated oncogenic lncRNA which represses miR-214 biogenesis and activates Wnt/β-catenin signaling, highlighting its potential as prognostic biomarker and therapeutic target for cervical cancer.

show abstract

“…Thyroid cancer (PTC) is the most common endocrine cancer. TRIM29 reduces miR-873-5p expression by upregulating LINC00152 to upregulate FN1, thereby promoting PTC migration and invasion ( 32 ). LINC00152 acts as a ceRNA miR-497 sponge, downregulating its downstream target brain-derived neurotrophic factor (BDNF) to promote cell proliferation, colony formation, migration, and invasion ( 31 ).…”

Section: Function and Mechanisms Of Linc00152 In Human Cancermentioning

confidence: 99%

Long non-coding RNA LINC00152 in cancer: Roles, mechanisms, and chemotherapy and radiotherapy resistance

Yao

Liu

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

Long non-coding RNA LINC00152 (cytoskeleton regulator, or LINC00152) is an 828-bp lncRNA located on chromosome 2p11.2. LINC00152 was originally discovered during research on hepatocarcinogenesis and has since been regarded as a crucial oncogene that regulates gene expression in many cancer types. LINC00152 is aberrantly expressed in various cancers, including gastric, breast, ovarian, colorectal, hepatocellular, and lung cancer, and glioma. Several studies have indicated that LINC00152 is correlated with cell proliferation, apoptosis, migration, invasion, cell cycle, epithelial-mesenchymal transition (EMT), chemotherapy and radiotherapy resistance, and tumor growth and metastasis. High LINC00152 expression in most tumors is significantly associated with poor patient prognosis. Mechanistic analysis has demonstrated that LINC00152 can serve as a competing endogenous RNA (ceRNA) by sponging miRNA, regulating the abundance of the protein encoded by a particular gene, or modulating gene expression at the epigenetic level. LINC00152 can serve as a diagnostic or prognostic biomarker, as well as a therapeutic target for most cancer types. In the present review, we discuss the roles and mechanisms of LINC00152 in human cancer, focusing on its functions in chemotherapy and radiotherapy resistance.

show abstract

TRIM29 inhibits miR-873-5P biogenesis via CYTOR to upregulate fibronectin 1 and promotes invasion of papillary thyroid cancer cells

Cited by 21 publications

References 45 publications

Label-Free Proteome Profiling for Lymphatic Metastasis in Papillary Thyroid Carcinoma

Label-Free Proteome Profiling for Lymphatic Metastasis in Papillary Thyroid Carcinoma

SPINT1-AS1 Drives Cervical Cancer Progression via Repressing miR-214 Biogenesis

Long non-coding RNA LINC00152 in cancer: Roles, mechanisms, and chemotherapy and radiotherapy resistance

Contact Info

Product

Resources

About