Tescalcin promotes highly invasive papillary thyroid microcarcinoma by regulating FOS/ERK signaling pathway

Zou, Xinyu; Zhou, Qian; Nie, Yongzhan; Gou, Junhe; Yang, Jing; Zhu, Jingqiang; Li, Zhihui; Gong, Yanping

doi:10.1186/s12885-022-09643-9

Cited by 6 publications

(5 citation statements)

References 32 publications

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“…demonstrated that TESC promoted the PTMC progression by regulating the c-Fos expression related to ERK signaling pathway and detected the expression of EMT pathway-related indicators (E-cad, N-cad, Vimentin, Snail) (12), which are consistent with our results, though an ATC cell line was used.…”

Section: Discussionsupporting

confidence: 91%

“…Moreover, BRAF V600E mutation activated the ERK1/2 signaling pathway contributing to DTC dedifferentiation (28). Recently, it has been reported that TESC/FOS/ERK1/2 signaling axis was involved in the growth and metastasis of PTC cells (12). Our results showed that TESC high expression positively correlated with TDS of DTC.…”

Section: Discussionsupporting

confidence: 59%

“…TESC can also regulate cancer progression, and its abnormal expression is associated with various malignant tumors, including non-small cell lung cancer, liver cancer, gastric cancer, and colorectal cancer (8)(9)(10)(11). It has been reported that TESC promoted papillary thyroid microcarcinoma (PTMC) progression by regulating c-Fos expression, which may be related to the ERK signaling pathway (12). Another study con rmed that lncRNA ROR mediates the TESC/ALDH1A1/TUBB3/PTEN axis, thereby promoting the development of PTC (13).…”

Section: Introductionmentioning

confidence: 99%

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TESC promotes differentiated thyroid cancer development by activating ERK and weakening NIS and radioiodine uptake

et al. 2023

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Most differentiated thyroid cancer (DTC) patients have a good prognosis after surgery, but radioiodine refractory differentiated thyroid cancer (RAIR-DTC) patients have a signi cantly reduced ve-year survival rate (< 60%) and a signi cantly increased recurrence rate (> 30%). This study aimed to clarify the tescalcin (TESC) role in promoting the malignant PTC progression and providing a potential target for RAIR-DTC treatment. MethodsWe analyzed TESC expression and clinicopathological characteristics using the Cancer Genome Atlas (TCGA) and performed qRT-PCR on tissue samples. TPC-1 and IHH4 proliferation, migration, and invasion were detected after transfection with TESC-RNAi. Using Western blot (WB), several EMT-related indicators were detected. Moreover, iodine uptake of TPC-1 and IHH4 after transfection with TESC-RNAi was detected. Finally, NIS, ERK1/2, and p-ERK1/2 levels were determined by WB. ResultsTESC was signi cantly upregulated in DTC tissues and positively correlated with BRAF V600E mutation based on data analysis from TCGA and our center. Reduced expression of TESC in both IHH-4 (BRAF V600E mutation) and TPC-1 (BRAF V600E wild type) cells signi cantly inhibited cell proliferation, migration, and invasion. It downregulated the EMT pathway markers Vimentin and N-cadherin, and increased E-cadherin. Moreover, TESC knockdown signi cantly inhibited ERK1/2 phosphorylation and decreased NIS expression in DTC cells, with a remarkably increased iodine uptake rate. ConclusionsTESC was highly expressed in DTC tissues and may have promoted metastasis through EMT and induced iodine resistance by downregulating NIS in DTC cells.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

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TESC promotes differentiated thyroid cancer development by activating ERK and weakening NIS and radioiodine uptake

et al. 2023

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“…However, we did not observe similar results because only TLR-4 was activated; this could be attributed to the unique microenvironment of mechanical stretch in the expanded skin. Furthermore, S100A9 could interact with TLR-4 to promote cell growth [ 46 ], thereby influencing the activation of downstream transcription factors such as Jun [ 47 ] and Fos [ 48 ]. Because S100A9 has been shown to promote tissue ECM deposition via the TLR-4/ERK1/2 pathway during skin expansion, the downstream regulator may be investigated.…”

Section: Discussionmentioning

confidence: 99%

S100 calcium-binding protein A9 promotes skin regeneration through toll-like receptor 4 during tissue expansion

Zhang,

Song,

et al. 2023

Burns &Amp; Trauma

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Background In plastic surgery, tissue expansion is widely used for repairing skin defects. However, low expansion efficiency and skin rupture caused by thin, expanded skin remain significant challenges in promoting skin regeneration during expansion. S100 calcium-binding protein A9 (S100A9) is essential in promoting wound healing; however, its effects on skin regeneration during tissue expansion remain unclear. The aim of the present study was to explore the role of S100A9 in skin regeneration, particularly collagen production to investigate its importance in skin regeneration during tissue expansion. Methods The expression and distribution of S100A9 and its receptors—toll-like receptor 4 (TLR-4) and receptor for advanced glycation end products were studied in expanded skin. These characteristics were investigated in skin samples of rats and patients. Moreover, the expression of S100A9 was investigated in stretched keratinocytes in vitro. The effects of S100A9 on the proliferation and migration of skin fibroblasts were also observed. TAK-242 was used to inhibit the binding of S100A9 to TLR-4; the levels of collagen I (COL I), transforming growth factor beta (TGF-β), TLR-4 and phospho-extracellular signal-related kinase 1/2 (p-ERK1/2) in fibroblasts were determined. Furthermore, fibroblasts were co-cultured with stretched S100A9-knockout keratinocytes by siRNA transfection and the levels of COL I, TGF-β, TLR-4 and p-ERK1/2 in fibroblasts were investigated. Additionally, the area of expanded skin, thickness of the dermis, and synthesis of COL I, TGF-β, TLR-4 and p-ERK1/2 were analysed to determine the effects of S100A9 on expanded skin. Results Increased expression of S100A9 and TLR-4 was associated with decreased extracellular matrix (ECM) in the expanded dermis. Furthermore, S100A9 facilitated the proliferation and migration of human skin fibroblasts as well as the expression of COL I and TGF-β in fibroblasts via the TLR-4/ERK1/2 pathway. We found that mechanical stretch-induced S100A9 expression and secretion of keratinocytes stimulated COL I, TGF-β, TLR-4 and p-ERK1/2 expression in skin fibroblasts. Recombined S100A9 protein aided expanded skin regeneration and rescued dermal thinning in rats in vivo as well as increasing ECM deposition during expansion. Conclusions These findings demonstrate that mechanical stretch promoted expanded skin regeneration by upregulating S100A9 expression. Our study laid the foundation for clinically improving tissue expansion using S100A9.

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Section: Introductionmentioning

confidence: 99%

Mechanism of TESC in the regulation of iodine resistance in differentiated thyroid carcinoma based on ERK-NIS axis

Guo

Cai

Song

et al. 2023

Preprint

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Purpose Most differentiated thyroid cancer (DTC) patients have a good prognosis after surgery, but radioiodine refractory differentiated thyroid cancer (RAIR-DTC) patients have a significantly reduced five-year survival rate (< 60%) and a significantly increased recurrence rate (> 30%). This study aimed to clarify the tescalcin (TESC) role in promoting the malignant PTC progression and providing a potential target for RAIR-DTC treatment. Methods We analyzed TESC expression and clinicopathological characteristics using the Cancer Genome Atlas (TCGA) and performed qRT-PCR on tissue samples. TPC-1 and IHH4 proliferation, migration, and invasion were detected after transfection with TESC-RNAi. Using Western blot (WB), several EMT-related indicators were detected. Moreover, iodine uptake of TPC-1 and IHH4 after transfection with TESC-RNAi was detected. Finally, NIS, ERK1/2, and p-ERK1/2 levels were determined by WB. Results TESC was significantly upregulated in DTC tissues and positively correlated with BRAF V600E mutation based on data analysis from TCGA and our center. Reduced expression of TESC in both IHH-4 (BRAF V600E mutation) and TPC-1 (BRAF V600E wild type) cells significantly inhibited cell proliferation, migration, and invasion. It downregulated the EMT pathway markers Vimentin and N-cadherin, and increased E- cadherin. Moreover, TESC knockdown significantly inhibited ERK1/2 phosphorylation and decreased NIS expression in DTC cells, with a remarkably increased iodine uptake rate. Conclusions TESC was highly expressed in DTC tissues and may have promoted metastasis through EMT and induced iodine resistance by downregulating NIS in DTC cells.

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Tescalcin promotes highly invasive papillary thyroid microcarcinoma by regulating FOS/ERK signaling pathway

Cited by 6 publications

References 32 publications

TESC promotes differentiated thyroid cancer development by activating ERK and weakening NIS and radioiodine uptake

TESC promotes differentiated thyroid cancer development by activating ERK and weakening NIS and radioiodine uptake

S100 calcium-binding protein A9 promotes skin regeneration through toll-like receptor 4 during tissue expansion

Mechanism of TESC in the regulation of iodine resistance in differentiated thyroid carcinoma based on ERK-NIS axis

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