Testicular orphan receptor 4 (TR4) promotes papillary thyroid cancer invasion via activating circ-FNLA/miR-149-5p/MMP9 signaling

Ouyang, Xiwu; Feng, Lemeng; Yao, Lei; Xiao, Yao; Hu, Xianyu; Zhang, Gewen; Liu, Guodong; Wang, Zhiming

doi:10.1016/j.omtn.2021.03.021

Cited by 16 publications

(12 citation statements)

References 34 publications

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“…Thyroid cancer (TC) is a prevalent endocrine malignancy worldwide, accounting for approximately 300,000 new cases in 2012 and 40,000 deaths [ 1 – 3 ]. TC is commonly classified into anaplastic TC, medullary TC, and differentiated TC [ 4 ]. Papillary TC (PTC) is an epithelial-derived differentiated TC that accounts for most TC cases [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Inhibits Papillary Thyroid Cancer Cell Proliferation by Regulating lncRNA LINC00691

Gao

et al. 2022

Analytical Cellular Pathology

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Papillary thyroid cancer (PTC) is a type of epithelial-derived differentiated TC that reportedly accounts for a majority of TCs. Curcumin, a polyphenolic compound and a member of the Zingiberaceae (ginger) family derived from turmeric plants, can exhibit anticancer effects. Herein, we aimed to investigate the effect of curcumin on PTC and elucidate underlying mechanisms. Accordingly, PTC B-CPAP cells were treated with curcumin, in combination with/without long noncoding RNA LINC00691 inhibition, to determine the effect of curcumin and its relationship with LINC00691 in PTC cells. We observed that curcumin treatment decreased B-CPAP cell proliferation and promoted apoptosis. Curcumin inhibited LINC00691 expression in B-CPAP cells. Curcumin administration or si-LINC00691 transfection alone promoted ATP levels, inhibited glucose uptake and lactic acid levels, and inhibited lactate dehydrogenase A and hexokinase 2 protein expression in B-CPAP cells, which were further enhanced by combination treatment. Moreover, curcumin administration or si-LINC00691 transfection alone inhibited p-Akt activity, further suppressed by combination treatment. Akt inhibition promoted apoptosis and suppressed the Warburg effect in B-CPAP cells. In conclusion, our findings indicate that curcumin promotes apoptosis and suppresses proliferation and the Warburg effect by inhibiting LINC00691 in B-CPAP cells. The precise molecular mechanism might be mediated through the Akt signaling pathway, providing a theoretical basis for the treatment of PTC with curcumin.

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Section: Introductionmentioning

confidence: 99%

Curcumin Inhibits Papillary Thyroid Cancer Cell Proliferation by Regulating lncRNA LINC00691

Gao

et al. 2022

Analytical Cellular Pathology

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“…Further, miR-149-5p was downregulated in the ISO-induced mouse hearts. Previous research has shown that the dysregulation of miR-149-5p is closely associated with malignant tumor progression, metastasis, and chemoresistance in gastric cancer (31)(32)(33), papillary thyroid cancer (34), colorectal cancer (35)(36)(37), and breast cancer (38). Additionally, miR-149-5p is also involved in the pathogenesis of inflammationassociated diseases, such as the PM 2.5 -induced inflammatory response (39), rheumatoid arthritis (40), and chronic obstructive pulmonary disease (41).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of LncRNA-HFRL expression induces cardiomyocyte inflammation, proliferation, and fibrosis via the sequestering of miR-149-5p-mediated collagen 22A inhibition

Teng

Tian

et al. 2022

Ann Transl Med

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Background Long non-coding ribonucleic acids (lncRNAs) are believed to play crucial roles in cardiovascular diseases; however, details of the underlying mechanisms by which this occurs remain unclear. Methods A mouse heart failure (HF) model was established using isoproterenol (ISO), and confirmed by immunostaining and echocardiography. RNA-sequencing was performed to screen the differential lncRNA expression profiles and heart failure relative lncRNA (HFRL) was selected as the target which was validated by quantitative real-time polymerase chain reaction (qRT-PCR). In HL-1 cells, the cardiac function, inflammatory, and fibrosis-related genes expression changes were examined by qRT-PCR after silencing of HFRL by lentivirus. Meanwhile, Cell Counting Kit-8 (CCK-8) assays were used to detect the effects of HFRL on the cell proliferation and viability. Reactive oxygen species (ROS) assays were also used to explore the role of HFRL in oxidative damage. Next, bioinformatics analysis was conducted to predict the potential binding microRNAs (mmu-miR-149-5p) to HFRL, which was confirmed by RNA-pulldown assays. The target gene of miR-149-5p was also predicted and further validated by Dual-luciferase reporter assays, qRT-PCR, and western blot. To investigate the synergistic regulatory effect of HFRL and miR-149-5p, HL-1 cells were infected with the lentivirus of HFRL with or without simultaneous knockdown of miR-149-5p. Then, qRT-PCR and western blot were used to examine cardiac function, inflammatory, and fibrosis-related gene expression changes, respectively. In HL-1 cells, CCK-8 assays were performed to detect the proliferation and viability. ROS assays were used to explore the oxidative damage. Results The administration of ISO induced mice fibrosis, inflammation, and HF. The in-vitro results showed that knockdown of HFRL suppressed cardiomyocyte proliferation and viability, attenuated inflammatory, cardiac function, and fibrosis-related gene expression, and promoted oxidative damage. HFRL was found to bind to mmu-miR-149-5p and inversely target the 3'-untranscripted region of the collagen 22A1 gene. Thus, HFRL affected cardiomyocyte inflammation, proliferation, viability, oxidative damage, and pro-fibrotic function via sequestration to miR-149-5p. Conclusions The HFRL/miR-149-5p axis plays an important role in regulating cardiac inflammation, proliferation, and fibrosis via a synergistic effect, which suggests that HFRL might be a novel target for HF.

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“…Binding of circ-FLNA with this miRNA releases MMP9 from the inhibitory effects of miR-149-5p. Thus, the TR4/circ-FLNA/miR-149-5p/MMP9 axis has been identified as an important player in the pathogenesis of papillary thyroid cancer [ 16 ].…”

Section: Cell Line Studiesmentioning

confidence: 99%

A Review on the Role of miR-149-5p in the Carcinogenesis

Ghafouri‐Fard

Khoshbakht

Hussen

et al. 2021

IJMS

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miR-149 is an miRNA with essential roles in carcinogenesis. This miRNA is encoded by the MIR149 gene on 2q37.3. The miR-149 hairpin produces miR-149-5p and miR-149-3p, which are the “guide” and the sister “passenger” strands, respectively. Deep sequencing experiments have shown higher prevalence of miR-149-5p compared with miR-149-3p. Notably, both oncogenic and tumor suppressive roles have been reported for miR-149-5p. In this review, we summarize the impact of miR-149-5p in the tumorigenesis and elaborate mechanisms of its involvement in this process in a variety of neoplastic conditions based on three lines of evidence, i.e., in vitro, in vivo and clinical settings.

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Testicular orphan receptor 4 (TR4) promotes papillary thyroid cancer invasion via activating circ-FNLA/miR-149-5p/MMP9 signaling

Cited by 16 publications

References 34 publications

Curcumin Inhibits Papillary Thyroid Cancer Cell Proliferation by Regulating lncRNA LINC00691

Curcumin Inhibits Papillary Thyroid Cancer Cell Proliferation by Regulating lncRNA LINC00691

Enhancement of LncRNA-HFRL expression induces cardiomyocyte inflammation, proliferation, and fibrosis via the sequestering of miR-149-5p-mediated collagen 22A inhibition

A Review on the Role of miR-149-5p in the Carcinogenesis

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