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Knockdown of long non?coding RNA CCAT2 suppresses the progression of thyroid cancer by inhibiting the Wnt/??catenin pathway.

ABSTRACT: Thyroid cancer (TC) is one of the most common malignancies with a high mortality rate. Long non?coding RNA CCAT2 (CCAT2) participates in the occurrence and development of certain human cancers; however, whether it is involved in TC remains unclear. Thus, the present study investigated the role of CCAT2 in TC and the underlying mechanism. CCAT2 expression in both TC tissues and cell lines was examined by reverse transcription?quantitative PCR. CCAT2 expression was silenced in TC cell lines by a specific small interfering (si)RNA against CCAT2 (si?CCAT2). The effects of CCAT2 silencing on TC cell proliferation were detected by CCK?8 and colony formation assays. Cell cycle and apoptosis of the treated TC cells were assessed by flow cytometry. Wound healing and Transwell assays were performed to detect the effects of si?CCAT2 on the migration and invasion of TC cells. Apoptosis?related proteins and Wnt/??catenin cascade?associated agents were examined by western blotting. The interaction between CCAT2 and the Wnt/??catenin pathway in the transfected cells was detected by performing a dual?luciferase reporter assay. CCAT2 expression was increased in TC tissue samples and cell lines compared with the controls. Tissue CCAT2 level was associated with T stage and tumor?node?metastasis stage of TC. Silencing CCAT2 inhibited TC cell proliferation, migration and invasion, and promoted TC cell cycle arrest and apoptosis. Furthermore, CCAT2 knockdown suppressed the activity of the Wnt/??catenin cascade in TC cells treated with lithium chloride. In summary, the present study demonstrated that CCAT2 knockdown suppresses TC progression via inactivating the Wnt/??catenin cascade, indicating that suppressing CCAT2 and the Wnt/??catenin signaling pathway may be a promising therapeutic strategy for treating TC.

SUBMITTER: Xin S

PROVIDER: S-EPMC7595661 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Knockdown of long non‑coding RNA CCAT2 suppresses the progression of thyroid cancer by inhibiting the Wnt/β‑catenin pathway.

Xin Suping S Ye Xinhua X

International journal of molecular medicine 20201019 6

Thyroid cancer (TC) is one of the most common malignancies with a high mortality rate. Long non‑coding RNA CCAT2 (CCAT2) participates in the occurrence and development of certain human cancers; however, whether it is involved in TC remains unclear. Thus, the present study investigated the role of CCAT2 in TC and the underlying mechanism. CCAT2 expression in both TC tissues and cell lines was examined by reverse transcription‑quantitative PCR. CCAT2 expression was silenced in TC cell lines by a s ...[more]

PMID: 33125134

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Project description:BackgroundAlthough there are many treatments for breast cancer, such as surgery, radiotherapy, chemotherapy, estrogen receptor antagonists, immune checkpoint inhibitors and so on. However, safer and more effective therapeutic drugs for breast cancer are needed. Sinensetin, a safer therapeutic drugs, come from citrus species and medicinal plants used in traditional medicine, while its role and underlying mechanism in breast cancer remain unclear. Our study aimed to investigate the role and mechanism of sinensetin in breast cancer.MethodsCell Counting Kit-8 (CCK-8) was used to determine the safe concentration of sinensetin in MCF-10A, MCF7 and MDA-MB-231 cells; 120 μM sinensetin was used in subsequent experiments. Real time polymerase chain reaction (RT-PCR), Western blotting, Terminal Deoxynucleotidyl Transferase mediated dUTP Nick-End Labeling (TUNEL) apoptosis assay, Transwell invasion assay and Clone formation assay were used in this study to determine cell viability, mRNA expression, protein levels, apoptosis, proliferation, invasion and so on.ResultsHerein, our results showed that 120 μM sinensetin suppressed the cell viability and promoted apoptosis of MCF7 and MDA-MB-231 cells. Treatment with 120 µM sinensetin for 24 h showed no significant toxicity to normal mammary cells; 120 μM sinensetin decreased cell proliferation, invasion, and epithelial-mesenchymal transition (EMT), and downregulated β-catenin, lymphatic enhancing factor 1 (LEF1), T-cell factor (TCF) 1/TCF7, and TCF3/TCF7L1 expression in MCF7 and MDA-MB-231 cells. The Wnt agonist SKL2001 reversed the inhibitory effect of sinensetin on cell survival, metastasis, and EMT. Sinensetin-induced downregulation of β-catenin, LEF1, and TCF1/TCF7 expression were upregulated by SKL2001 in MCF7 and MDA-MB-231 cells.ConclusionsIn summary, sinensetin suppressed the metastasis of breast cancer cell via inhibition of Wnt/β-catenin pathway and there were no adverse effects on normal breast cells. Our study confirmed the role of sinensetin in breast cancer cells and provided a better understanding of the underlying mechanism.

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Knockdown of long non?coding RNA CCAT2 suppresses the progression of thyroid cancer by inhibiting the Wnt/??catenin pathway.

Publications

Knockdown of long non‑coding RNA CCAT2 suppresses the progression of thyroid cancer by inhibiting the Wnt/β‑catenin pathway.

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