Association between Circulating Fibroblast Growth Factor 21 and Aggressiveness in Thyroid Cancer

Kang, Yea Eun; Kim, Jung Tae; Lim, Mi Ae; Oh, Chahyun; Liu, Lihua; Jung, Seung-Hyun; Won, Ho-Ryun; Lee, Kyung-Min; Chang, Jae Won; Yi, Hyon‐Seung; Kim, Hyun Jin; Ku, Bon Jeong; Shong, Minho; Koo, Bon Seok

doi:10.3390/cancers11081154

Cited by 28 publications

(30 citation statements)

References 64 publications

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“…Kang et al showed that FGF21 was highly expressed in papillary thyroid carcinoma serum and that its expression level was positively correlated with the tumor stage, vascular lymphatic invasion, and recurrence. The underlying mechanism proposed was that FGF21 promotes tumor growth and invasion through the regulation of the signal axis of the FGFR pathway [49]. Studies in China reported that the transient silencing of FGF21 increased the sorafenib-induced inhibition of hepatocellular carcinoma cell proliferation [50].…”

Section: Discussionmentioning

confidence: 99%

FANCD2 knockdown with shRNA interference enhances the ionizing radiation sensitivity of nasopharyngeal carcinoma CNE-2 cells

Bao

Feng

Zhao

et al. 2021

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Fanconi anemia complementation group D2 (FANCD2) has been associated with the sensitivity of tumor cells to DNA crosslinking damaging agents in certain solid tumors. However, its role in nasopharyngeal carcinoma (NPC) is still unclear. In the present study, the role of FANCD2 in the response of NPC CNE-2 cells to radiation was investigated. A CNE-2 cell model with stable FANCD2 silencing was constructed by lentiviral transfection. Fluorescence quantitative PCR and western blotting were used to evaluate FANCD2 expression in CNE-2 cells. The biological impact of FANCD2 silencing on the response of CNE-2 cells to radiation was investigated in vitro and in vivo. The microarray technology, western blotting, and immunohistochemistry were used to analyze the proteins involved in related pathways after irradiation to investigate the underlying mechanism. Lentivirus-mediated shRNA interference stably silenced the FANCD2 gene in CNE-2 cells. In vitro, in the FANCD2-silenced group, cell proliferation was significantly inhibited, apoptosis was increased, and the cell cycle was arrested at the G2/M phase after irradiation. In vivo, FANCD2 s ilencing slowed tumor growth, as the volume and weight of the xenograft tumors were significantly decreased. Both in vitro and in vivo, the differentially expressed genes NUPR1, FLI1, and FGF21 were downregulated in the FANCD2-silenced group. Our results show that FANCD2 silencing affected the sensitivity of CNE-2 cells to ionizing radiation by regulating cell proliferation, apoptosis, and cell cycle distribution. The mechanism might be associated with changes in NUPR1, FLI1, and FGF21 protein expression due to the FANCD2 silencing. This study provides a promising target for NPC radiotherapy.

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Section: Discussionmentioning

confidence: 99%

FANCD2 knockdown with shRNA interference enhances the ionizing radiation sensitivity of nasopharyngeal carcinoma CNE-2 cells

Bao

Feng

Zhao

et al. 2021

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“…Treatment of PTC cell lines with recombinant FGFR1 leads to FGFR pathway signaling activation, leading to ERK and AKT phosphorylation, EMT, and to the development of a more aggressive phenotype of tumor cells. Thus, FGFR1 can promote invasion and migration of PTC cells ( 136 ). Parascandolo et al showed that mesenchymal stem cell (MSC) cultures derived from non-tumorigenic thyroid tissues and from PTCs, exposed to cancer cell-released factors, are able to differentiate into a multitude of cell types, including CAFs, which eventually support tumor progression.…”

Section: Influence Of the Tumor Microenvironment On Tcscsmentioning

confidence: 99%

Cancer Stem Cells in Thyroid Tumors: From the Origin to Metastasis

et al. 2020

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Thyroid tumors are extremely heterogeneous varying from almost benign tumors with good prognosis as papillary or follicular tumors, to the undifferentiated ones with severe prognosis. Recently, several models of thyroid carcinogenesis have been described, mostly hypothesizing a major role of the thyroid cancer stem cell (TCSC) population in both cancer initiation and metastasis formation. However, the cellular origin of TCSC is still incompletely understood. Here, we review the principal epigenetic mechanisms relevant to TCSC origin and maintenance in both well-differentiated and anaplastic thyroid tumors. Specifically, we describe the alterations in DNA methylation, histone modifiers, and microRNAs (miRNAs) involved in TCSC survival, focusing on the potential of targeting aberrant epigenetic modifications for developing novel therapeutic approaches. Moreover, we discuss the bidirectional relationship between TCSCs and immune cells. The cells of innate and adaptive response can promote the TCSC-driven tumorigenesis, and conversely, TCSCs may favor the expansion of immune cells with protumorigenic functions. Finally, we evaluate the role of the tumor microenvironment and the complex cross-talk of chemokines, hormones, and cytokines in regulating thyroid tumor initiation, progression, and therapy refractoriness. The re-education of the stromal cells can be an effective strategy to fight thyroid cancer. Dissecting the genetic and epigenetic landscape of TCSCs and their interactions with tumor microenvironment cells is urgently needed to select more appropriate treatment and improve the outcome of patients affected by advanced differentiated and undifferentiated thyroid cancers.

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“…In addition, FGF21 is also expressed in other tissues such as the pancreas, adipose tissue, muscle, and kidney under pathological and stress conditions 11 . Recent studies have also revealed that FGF21 is associated with the occurrence and development of tumors such as colon cancer 12 , thyroid cancer 11 , and liver cancer 13 . However, its role in PCa has not been reported to date.…”

Section: Introductionmentioning

confidence: 99%

FGF21 facilitates autophagy in prostate cancer cells by inhibiting the PI3K–Akt–mTOR signaling pathway

Dai

Hu²,

Zhang

et al. 2021

Cell Death Dis

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Fibroblast growth factor 21 (FGF21) plays an important role in regulating glucose and lipid metabolism, but its role in cancer is less well-studied. We aimed to investigate the action of FGF21 in the development of prostate cancer (PCa). Herein, we found that FGF21 expression was markedly downregulated in PCa tissues and cell lines. FGF21 inhibited the proliferation and clone formation of LNCaP cells (a PCa cell line) and promoted apoptosis. FGF21 also inhibited PCa cell migration and invasiveness. The Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed that FGF21 was related to autophagy and the phosphatidylinositol 3-kinase–Akt kinase–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. Mechanistically, FGF21 promoted autophagy in LNCaP cells by inhibiting the PI3K–Akt–mTOR–70S6K pathway. In addition, FGF21 inhibited PCa tumorigenesis in vivo in nude mice. Altogether, our findings show that FGF21 inhibits PCa cell proliferation and promoted apoptosis in PCa cells through facilitated autophagy. Therefore, FGF21 might be a potential novel target in PCa therapy.

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Association between Circulating Fibroblast Growth Factor 21 and Aggressiveness in Thyroid Cancer

Cited by 28 publications

References 64 publications

FANCD2 knockdown with shRNA interference enhances the ionizing radiation sensitivity of nasopharyngeal carcinoma CNE-2 cells

FANCD2 knockdown with shRNA interference enhances the ionizing radiation sensitivity of nasopharyngeal carcinoma CNE-2 cells

Cancer Stem Cells in Thyroid Tumors: From the Origin to Metastasis

FGF21 facilitates autophagy in prostate cancer cells by inhibiting the PI3K–Akt–mTOR signaling pathway

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