Retracted: Silencing of cystatin SN abrogates cancer progression and stem cell properties in papillary thyroid carcinoma.
Retracted: Silencing of cystatin SN abrogates cancer progression and stem cell properties in papillary thyroid carcinoma.
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DOI：
10.1002/2211-5463.13221
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发表时间：
2021-08
期刊：
影响因子：
2.6
通讯作者：
Song T
中科院分区：
文献类型：
--
作者：
Ding J;Wang X;Gao J;Song T
甲状腺乳头状癌（PTC）约占全球甲状腺癌总数的80%。虽然早期PTC的预后良好，但晚期PTC患者的5年生存率仍然很差。半胱氨酸蛋白酶抑制剂SN（cystatin 1，CST 1）促进多种癌症的进展，但其在调节PTC发病机制中的作用仍在很大程度上未知。在本研究中，我们通过真实的实时定量PCR和western blot分析来测量PTC临床组织和细胞系中的CST 1表达水平，并且我们进行功能获得和丧失实验来检查CST 1对PTC细胞生长、侵袭、迁移、上皮-间充质转化和干性的影响。使用体内荷瘤裸鼠模型评估致瘤性。与正常对照组相比，PTC组织和细胞中的CST 1表达均显著上调（P <0.05），且CST 1表达水平高的PTC患者预后差（P <0.05）。此外，在体内和体外，CST 1消融抑制PTC细胞的生长（P < 0.05）。CST 1基因沉默抑制PTC细胞的运动和上皮-间质转化（P < 0.05），而CST 1基因过表达则抑制PTC细胞的早期功能。值得注意的是，在PTC细胞中，上调CST 1促进细胞球体形成（P < 0.05）并增加干细胞特征的表达水平（P < 0.05）。总的来说，这些研究结果表明，CST 1作为癌基因的功能，以促进癌症的发展和促进PTC细胞中的癌症干细胞特性，增加我们对PTC发病机制的理解，并可能有助于开发潜在的治疗策略。CST 1的上调促进乳头状甲状腺癌（PTC）细胞中的细胞增殖、运动性、上皮-间充质转化和干细胞性，这加速了PTC细胞向PTC干细胞的转化，从而导致PTC恶性。
Papillary thyroid carcinoma (PTC) accounts for approximately 80% of total thyroid cancers worldwide. Although the prognosis for early‐stage PTC is favorable, the 5‐year survival rate of patients with late‐stage PTC is still very poor. Cystatin SN (cystatin 1, CST1) facilitates the progression of multiple cancers, but its role in regulating PTC pathogenesis is still largely unknown. In this study, we measured the expression levels of CST1 in PTC clinical tissues and cell lines by real‐time quantitative PCR and western blot analysis, and we performed gain‐ and loss‐of‐function experiments to examine the effects of CST1 on PTC cell growth, invasion, migration, epithelial–mesenchymal transition and stemness. Tumorigenicity was assessed using in vivo tumor‐bearing nude mouse models. As expected, upregulated CST1 was observed in PTC tissues (P < 0.05) and cells, compared with their normal counterparts (P < 0.05); furthermore, patients with PTC with higher levels of CST1 exhibited unfavorable prognosis (P < 0.05). In addition, CST1 ablation inhibited PTC cell growth (P < 0.05) in vivo and in vitro. Silencing of CST1 also inhibited cell motility and epithelial–mesenchymal transition in PTC cells (P < 0.05), whereas CST1 overexpression had the opposite effects on the earlier cellular functions. Notably, up‐regulation of CST1 promoted cell spheroid formation (P < 0.05) and increased the expression levels of stemness signatures (P < 0.05) in PTC cells. Collectively, these findings suggest that CST1 functions as an oncogene to facilitate cancer development and promote cancer stem cell properties in PTC cells, increasing our understanding of PTC pathogenesis mechanisms and possibly aiding in the development of potential therapeutic strategies. Up‐regulation of CST1 promotes cell proliferation, motility, epithelial–mesenchymal transition and stemness in papillary thyroid carcinoma (PTC) cells, which accelerates the transition from PTC cells to PTC stem cells, thereby contributing to PTC malignancy.
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影响因子：
9
作者：
Oh BM;Lee SJ;Cho HJ;Park YS;Kim JT;Yoon SR;Lee SC;Lim JS;Kim BY;Choe YK;Lee HG
通讯作者：
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影响因子：
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作者：
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10.1016/j.biocel.2019.02.010
发表时间：
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作者：
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5
作者：
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影响因子：
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