Curcumin inhibits the viability, migration and invasion of papillary thyroid cancer cells by regulating the miR‑301a‑3p/STAT3 axis

Abstract

Thyroid cancer is one of the most common malignant tumors, and the mortality rate associated with thyroid cancer has been increasing annually. Curcumin has been reported to exert an antitumor effect on papillary thyroid cancer (PTC), and the identification of additional mechanisms underlying the anticancer effect of curcumin on PTC requires further investigation. The present study aimed to explore the effects of curcumin on the viability, migration and invasion of PTC cells. TPC-1 cells were incubated with different concentrations of curcumin, and then, cell viability, migration and invasion, and wound healing were examined by CCK-8, Transwell and wound healing assays, respectively. Subsequently, microRNA (miR)-301a-3p mimics, miR-301a-3p inhibitors and signal transducer and activator of transcription (STAT)3 overexpression vector were transfected into TPC-1 cells, and cell viability, migration, and invasion were reassessed in these transfected cells. Matrix metallopeptidase (MMP)-2, MMP-9, epithelial-mesenchymal transition (EMT)-related markers, and Janus kinase (JAK)/STAT signaling pathway components were assessed by western blot analysis. Curcumin significantly inhibited cell viability, migration and invasion and downregulated MMP-2, MMP-9 and EMT marker expression. Additionally, curcumin decreased STAT3 expression by upregulating miR-301a-3p expression, and the inhibition of miR-301a-3p and the overexpression of STAT3 reversed the effects of curcumin on cell viability, migration and invasion, and MMP-2, MMP-9 and EMT marker expression in TPC-1 cells. Furthermore, curcumin suppressed the JAK/STAT signaling pathway through the miR-301a-3p/STAT3 axis. The data of the present study indicated that curcumin could inhibit the viability, migration and invasion of TPC-1 cells by regulating the miR-301a-3p/STAT3 axis. These findings may provide a possible strategy for the clinical treatment of PTC.

Effects and Mechanisms of Curcumin for the Prevention and Management of Cancers: An Updated Review

“…The potential mechanisms might be attenuating lncRNA H19 [ 29 ]. Another study suggested that the migration and invasion of papillary thyroid cancer TPC-1 and BCPAP-R cells were suppressed by curcumin through up-regulation of miR-301a-3p [ 78 ]. Furthermore, curcumin significantly inhibited wound closure and invasion of pancreatic cancer Patu8988 and Panc-1 cells, which was mediated by inhibiting neural precursor cell expressed developmentally down-regulated protein 4 (NEDD4)/Akt/mTOR pathway [ 90 ].…”

Curcumin and its nano-formulations: Defining triple-negative breast cancer targets through network pharmacology, molecular docking, and experimental verification

“…STAT3 is pivotal in regulating the progression, metastasis, and immune evasion of TNBC ( Qin et al, 2019 ). In fact, CUR has been reported to suppress the proliferation, migration, and invasion of cancer cells by suppressing STAT3 activity ( Datta et al, 2018 ; Liang et al, 2021 ). AKT1 increases the proliferation and survival of cancer cells and AKT inhibitors could control the progression, drug resistance, and immunosuppression of breast cancer ( Hinz and Jücker, 2019 ; Jabbarzadeh Kaboli et al, 2020 ).…”

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“…Recent studies show that curcumin may affect the EMT process and MMPs secretion through miRNA- and lncRNA-mediated mechanisms. For example, curcumin may inhibit the expression of JAK/STAT signaling effector proteins p-JAK1, JAK1, p-JAK2, JAK2, p-JAK3, JAK3, p-STAT1, STAT1, p-STAT2 and STAT2 by upregulating miR-301a-3p, thus affecting the vitality of thyroid cancer cells TPC-1 [ 48 ]. Cai et al [ 49 ] found that lncRNA H19 can activate the EMT process, as well as invasion and metastasis of breast cancer MCF 7/TAMR cells, whereas curcumin can reverse these phenotypes induced by lncRNA H19.…”