lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line

Abstract

Thyroid cancer is a common malignant tumor. Long non-coding RNA colon cancer-associated transcript 1 (lncRNA CCAT1) is highly expressed in many cancers; however, the molecular mechanism of CCAT1 in thyroid cancer remains unclear. Hence, this study aimed to investigate the effect of CCAT1 on human thyroid cancer cell line FTC-133. FTC-133 cells were transfected with CCAT1 expressing vector, CCAT1 shRNA, miR-143 mimic, and miR-143 inhibitor, respectively. After different treatments, cell viability, proliferation, migration, invasion, and apoptosis were measured. Moreover, the regulatory relationship of CCAT1 and miR-143, as well as miR-143 and VEGF were tested using dual-luciferase reporter assay. The relative expressions of CCAT1, miR-143, and VEGF were tested by qRT-PCR. The expressions of apoptosis-related factors and corresponding proteins in PI3K/AKT and MAPK pathways were analyzed using western blot analysis. The results suggested that CCAT1 was up-regulated in the FTC-133 cells. CCAT1 suppression decreased FTC-133 cell viability, proliferation, migration, invasion, and miR-143 expression, while it increased apoptosis and VEGF expression. CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143. Moreover, CCAT1 activated PI3K/AKT and MAPK signaling pathways through inhibition of miR-143. This study demonstrated that CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143. These findings will provide a possible target for clinical treatment of thyroid cancer.

LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition

“…5,27 The signaling pathway activation plays a critical role in podocyte cytoskeleton structure stabilization and podocyte apoptosis inhibition. 17,25 Therefore, inhibition of CCAT1 in this study might regulate the activation of PI3K/Akt activation by either one of them, but this needs further investigation. It has been shown that the PI3K/Akt pathway can be regulated by the targets of CCAT1, including miR-143 and EGFR.…”

“…17 By enhancing the stability of targeting protein, CCAT1 upregulates the expression level of the protein, such as Livin, a protein generally regarded as an apoptosis inhibitor in various malignancie. 12,25,26 All these indicate that CAAT1 is a master regulator, and can resultantly affect a variety of cellular signaling pathways, including Wnt/β-catenin, MEK/ERK1/2, and PI3K/AKT signaling pathways. 12,25,26 All these indicate that CAAT1 is a master regulator, and can resultantly affect a variety of cellular signaling pathways, including Wnt/β-catenin, MEK/ERK1/2, and PI3K/AKT signaling pathways.…”

LncRNA CCAT1 Promotes Prostate Cancer Cell Proliferation by Interacting with DDX5 and MIR-28-5P

“…K, CCAT1 exhibited different regulatory mechanisms in cellular nuclei and cytoplasm to promote malignant progression of prostate cancer. activate the PI3K/AKT and MAPK signaling pathways (27), as well as in non-small cell lung cancer, CCAT1 stimulates the elements of the Wnt signaling pathway by blocking Let-7c function (28). Similarly, the CCAT1/MIR-181a-5P/HOXA1 axis was shown to exert an oncogenic role in multiple myeloma (29).…”

LncRNA MAFG‐AS1 facilitates the migration and invasion of NSCLC cell via sponging miR‐339‐5p from MMP15

“…For instance, lncRNA ZEB1‐AS1 is related with poor prognosis in NSCLC and promotes cancer cell metastasis (Liu et al, ). Furthermore, CCAT1 promotes cell growth, migration, and invasion of thyroid carcinoma cell via down‐regulation of miR‐143 (Yang et al, ). In ER‐positive breast cancer, MIAT is estrogen‐responsive and promotes estrogen‐induced growth of cancer cell (Luan et al, ).…”