AbstractThe global incidence of thyroid cancer has increased over recent decades. Papillary thyroid cancer (PTC) is the most common type of thyroid cancer and accounts for nearly 90% of all cases. Typically, PTC has a good prognosis. However, some PTC variants exhibit more aggressive behaviour, which significantly increases the risk of postoperative recurrence.

摘要近几十年来，全球甲状腺癌的发病率有所增加。甲状腺乳头状癌（PTC）是最常见的甲状腺癌类型，占所有病例的近90%。通常，PTC预后良好。然而，一些PTC变体表现出更具攻击性的行为，这显着增加了术后复发的风险。

Over the past decade, the high metastatic potential of PTC has drawn the attention of many researchers and these studies have provided useful molecular markers for improved diagnosis, risk stratification and clinical approaches. The aim of this review is to discuss the progress in epidemiology, metastatic features, risk factors and molecular mechanisms associated with PTC aggressiveness.

在过去的十年中，PTC的高转移潜能引起了许多研究人员的关注，这些研究为改进诊断，风险分层和临床方法提供了有用的分子标记。本综述的目的是讨论与PTC侵袭性相关的流行病学，转移特征，危险因素和分子机制的进展。

We present a detailed picture showing that epithelial-to-mesenchymal transition, cancer metabolic reprogramming, alterations in important signalling pathways, epigenetic aberrations and the tumour microenvironment are crucial drivers of PTC metastasis. Further research is needed to more fully elucidate the pathogenesis and biological behaviour underlying the aggressiveness of PTC..

我们提供了一张详细的图片，显示上皮-间质转化，癌症代谢重编程，重要信号通路的改变，表观遗传畸变和肿瘤微环境是PTC转移的关键驱动因素。需要进一步的研究来更全面地阐明PTC侵袭性的发病机制和生物学行为。。

Facts

事实

The incidence of PTC has increased globally in recent years.

近年来，全球PTC的发病率有所增加。

Some PTCs exhibit aggressive behaviours, which significantly increase the risk of postoperative recurrence and metastasis.

一些PTC表现出攻击性行为，这显着增加了术后复发和转移的风险。

The pathogenesis and regulatory networks involved in the aggressiveness of PTC are complicated and include epithelial-to-mesenchymal transition, tumour cell metabolic reprogramming, signalling pathways and epigenetic modifications.

PTC侵袭性的发病机制和调控网络很复杂，包括上皮细胞向间充质细胞的转化，肿瘤细胞的代谢重编程，信号通路和表观遗传修饰。

Open questions

开放式问题

What are the characteristics of the high aggressiveness in PTC?

PTC中高攻击性的特征是什么？

What are the risk factors increasing the aggressive behaviours of PTC?

什么是增加PTC攻击行为的风险因素？

How do these regulatory cellular networks drive the aggressiveness of PTC?

这些监管蜂窝网络如何推动PTC的侵略性？

IntroductionThyroid cancer is the most common endocrine malignancy, and its incidence has been rapidly increasing globally. In a previous study, the worldwide morbidity, mortality and disability-adjusted life-years of patients with thyroid cancer and the age-standardised incidence rate increased by 60– to 200% from 1990 to 2017 [1].

引言甲状腺癌是最常见的内分泌恶性肿瘤，其发病率在全球范围内迅速增加。在之前的一项研究中，从1990年到2017年，甲状腺癌患者的全球发病率，死亡率和残疾调整生命年以及年龄标准化发病率增加了60%至200%[1]。

In China, the age-standardised morbidity of thyroid cancer has tripled in the past decade [2]. Thyroid cancer predominantly affects women; it is the most common malignant tumour in women aged <30 years [3]. In every country, morbidity in women is approximately three times greater than that in men [4].

在中国，甲状腺癌的年龄标准化发病率在过去十年中增加了三倍（2）。甲状腺癌主要影响女性；它是30岁以下女性最常见的恶性肿瘤（3）。在每个国家，女性的发病率大约是男性的三倍（4）。

According to the latest Chinese cancer statistics, thyroid cancer is the fourth most common type of cancer in women in China, with morbidity increasing by 12.4% per year [2, 5].The majority of thyroid tumours originate from thyroid follicular epithelial cells, whereas 3–5% of thyroid cancers originate from parafollicular cells.

。大多数甲状腺肿瘤起源于甲状腺滤泡上皮细胞，而3-5%的甲状腺癌起源于滤泡旁细胞。

Follicular cell-derived cancers can be further subdivided into papillary carcinoma, follicular carcinoma, poorly differentiated carcinoma (insular carcinoma) and anaplastic (undifferentiated) carcinoma [6]. Among them, PTC and follicular thyroid cancer (FTC) are two histological types of differentiated thyroid cancer (DTC) [7].

滤泡细胞来源的癌症可进一步细分为乳头状癌，滤泡癌，低分化癌（岛状癌）和间变性（未分化）癌（6）。其中，PTC和滤泡性甲状腺癌（FTC）是分化型甲状腺癌（DTC）的两种组织学类型。

PTC is the most common type of cancer, accounting for 89.1% of all thyroid cancers and almost all newly diagnosed thyroid cancers [8, 9]. In contrast, medullary thyroid cancer (MTC), anaplastic thyroid cancer (ATC) and poorly differentiated thyroid cancer (PDTC) are rare but highly malignant [10]. According to the cancer statistics of the United States, MTC, which is a rare malignancy, accounts for 1–2% of all thyroid cancers [11].

PTC是最常见的癌症类型，占所有甲状腺癌和几乎所有新诊断的甲状腺癌的89.1%[8，9]。相比之下，甲状腺髓样癌（MTC），甲状腺未分化癌（ATC）和低分化甲状腺癌（PDTC）是罕见但高度恶性的（10）。根据美国癌症统计数据，MTC是一种罕见的恶性肿瘤，占所有甲状腺癌的1-2%[11]。

More than 15–20% of MTC patients develop distant metastases and ha.

超过15-20%的MTC患者发生远处转移和ha。

TGF-β

TGF-β

The transforming growth factor-β (TGF-β) signalling pathway plays a critical role in initiating EMT. In PTC, sineoculis homeobox homologue 1 (SIX1) promotes this pathway, facilitating the acquisition of motility and migratory abilities by PTC cells to penetrate the basement membrane and invade adjacent tissues, eventually resulting in distant metastases [84]..

转化生长因子-β（TGF-β）信号通路在启动EMT中起关键作用。在PTC中，sineoculis同源框同源物1（SIX1）促进了这一途径，促进了PTC细胞获得运动和迁移能力，穿透基底膜并侵入邻近组织，最终导致远处转移。。

Wnt

The Wnt signalling pathway is also involved in PTC progression. Tripartite motif 44 (TRIM44), a member of the TRIM family, is highly expressed in PTC. TRIM44 promotes the activation of the Wnt/β-catenin signalling pathway, inducing EMT and facilitating the proliferation, migration and aggressiveness of PTC cells [85].

Wnt信号通路也参与PTC进展。Triparty motif 44（TRIM44）是TRIM家族的成员，在PTC中高度表达。TRIM44促进Wnt/β-连环蛋白信号通路的激活，诱导EMT并促进PTC细胞的增殖，迁移和侵袭性。

Additionally, DOCK9 antisense RNA2 (DOCK9-AS2), an exosomal lncRNA derived from PTC cancer stem-like cells (PTC-CSCs), is highly expressed in PTC [86]. Mechanistically, DOCK9-AS2 enhances β-catenin expression via SP1 and miR-1972 to activate the Wnt/β-catenin pathway, inducing EMT and enhancing the progression of PTC [86]..

此外，DOCK9反义RNA2（DOCK9-AS2）是一种来源于PTC癌症干细胞样细胞（PTC CSCs）的外来体lncRNA，在PTC（86）中高度表达。从机制上讲，DOCK9-AS2通过SP1和miR-1972增强β-连环蛋白的表达，激活Wnt/β-连环蛋白途径，诱导EMT并增强PTC的进展。。

Notch

缺口

In many studies, the Notch pathway has been implicated as a driver of EMT. Downregulation of miR‐599 may induce EMT by activating the Notch signalling pathway and upregulating HEY2, thereby promoting the proliferation, migration and aggressiveness of PTC [87].

在许多研究中，Notch途径被认为是EMT的驱动因素。miR-599的下调可能通过激活Notch信号通路和上调HEY2诱导EMT，从而促进PTC的增殖、迁移和侵袭性。

Hh

小时

The hedgehog (Hh) signalling pathway is a vital mediator of PTC cell aggressiveness and metastasis. Low miR-431 expression activates the Hh signalling pathway by upregulating Gli1 expression, thereby facilitating EMT. During this process, the epithelial marker E-cadherin decreases, whereas the mesenchymal marker vimentin increases, thereby promoting PTC metastasis [88]..

刺猬（Hh）信号通路是PTC细胞侵袭性和转移的重要介质。低miR-431表达通过上调Gli1表达激活Hh信号通路，从而促进EMT。在此过程中，上皮标志物E-钙粘蛋白减少，而间充质标志物波形蛋白增加，从而促进PTC转移。。

PI3K/AKT

PI3K/AKT

The phosphoinositide 3-kinase (PI3K)/AKT signalling pathway can also induce EMT. Nectin cell adhesion molecule 4 (NECTIN4), a member of the NECTIN family, a group of Ca2+-independent immunoglobulin-like molecules, is significantly overexpressed in PTC and modulates EMT by activating the PI3K/AKT signalling pathway to drive PTC metastasis [89, 90]..

磷酸肌醇3-激酶（PI3K）/AKT信号通路也可以诱导EMT。Nectin细胞粘附分子4（NECTIN4）是Nectin家族的成员，是一组不依赖Ca2+的免疫球蛋白样分子，在PTC中显着过表达，并通过激活PI3K/AKT信号通路来调节EMT，从而驱动PTC转移[89，90]。。

EMT-inducing transcription factors (EMT-TFs)In this section, we discuss various EMT-TFs that activate signalling pathways to modulate EMT during PTC progression, including SNAIL1, the basic helix–loop–helix factor TWIST and the zinc finger E-box-binding homeobox factors ZEB1 and E47.The regulation of SNAIL1 and TWIST in PTC has been well documented.

EMT诱导转录因子（EMT-TFs）在本节中，我们讨论了在PTC进展过程中激活信号通路以调节EMT的各种EMT-TFs，包括SNAIL1，基本螺旋-环-螺旋因子TWIST和锌指E-box结合同源框因子ZEB1和E47。PTC中SNAIL1和TWIST的调节已被充分记录。

DDR2 overexpression induces EMT and promotes the metastasis and aggressiveness of PTC cells. This process is dependent on the upregulation of the SNAIL1 protein and the activation of extracellular signal-regulated kinase (ERK) 2 [91], whereas high expression of Sirtuin 6 (SIRT6) increases hypoxia-inducible factor-1α (HIF-1α) to regulate the expression of both SNAIL and TWIST.

DDR2过表达诱导EMT并促进PTC细胞的转移和侵袭性。这一过程依赖于SNAIL1蛋白的上调和细胞外信号调节激酶（ERK）2（91）的激活，而Sirtuin 6（SIRT6）的高表达增加缺氧诱导因子-1α（HIF-1α）以调节SNAIL和TWIST的表达。

HIF-1α can directly bind to the hypoxia-response element (HRE) in its promoter to upregulate SNAIL and TWIST. The overexpression of SNAIL and TWIST downregulates E-cadherin and upregulates vimentin to promote EMT and PTC progression [92, 93].ZEB1, another EMT-related TF, can inhibit cadherin 1 (CDH1) transcription and recruit other chromatin-modifying factors to their promoters, inducing the expression of genes encoding N-cadherin and vimentin and promoting EMT [83].

HIF-1α可以直接与其启动子中的缺氧反应元件（HRE）结合以上调SNAIL和TWIST。SNAIL和TWIST的过度表达下调E-钙粘蛋白并上调波形蛋白以促进EMT和PTC进展[92，93]。ZEB1是另一种与EMT相关的TF，可以抑制钙粘蛋白1（CDH1）的转录，并将其他染色质修饰因子募集到其启动子中，诱导编码N-钙粘蛋白和波形蛋白的基因的表达并促进EMT〔83〕。

ABC transporter A1 (ABCA1), a member of the ABC subfamily A, is involved in the reverse cholesterol transport pathway (RCT), which is crucial for regulating cellular cholesterol, phospholipid efflux and lipid homoeostasis [94]. The overexpression of ABCA1 promotes ZEB1 transcription by activating the ERK/Fra-1 pathway.

ABC转运蛋白A1（ABCA1）是ABC亚家族a的成员，参与胆固醇逆向转运途径（RCT），这对于调节细胞胆固醇、磷脂外排和脂质稳态至关重要。ABCA1的过表达通过激活ERK/Fra-1途径促进ZEB1转录。

This process is thought to drive PTC lung metastases [95]. Furthermore, taurine-upregulated gene 1 (TUG1), a lncRNA located on chromosome 22q12, is upregulated in PTC [96, 97]. Elevated expression of TUG1 can promote the EMT, proliferation, metastasis and aggressiveness of PT.

这个过程被认为是驱动PTC肺转移（95）。此外，牛磺酸上调基因1（TUG1），一种位于染色体22q12上的lncRNA，在PTC中上调[96，97]。TUG1的表达升高可以促进PT的EMT，增殖，转移和侵袭性。

miRNAs

微rna

miRNAs are a class of small noncoding regulatory RNAs 17–25 nucleotides in length. miRNAs are generated by Dicer, an RNase that processes hairpin-structured precursors (pre-miRNAs) into mature miRNAs [166]. In general, miRNAs recognise and bind to the 3’-untranslated region (3’-UTR) of target mRNAs to repress the expression of the target gene at the posttranscriptional level [167].

miRNA是一类长度为17-25个核苷酸的小型非编码调控RNA。。一般来说，miRNA识别并结合靶mRNA的3’-非翻译区（3’-UTR），在转录后水平上抑制靶基因的表达。

miRNAs play critical roles in the regulation of cancer biology, including the cell cycle, programmed cell death, cell invasion and metastasis, and angiogenesis, to drive tumour initiation and development [167]..

miRNA在癌症生物学的调节中起着关键作用，包括细胞周期，程序性细胞死亡，细胞侵袭和转移以及血管生成，以驱动肿瘤的发生和发展。。

In PTC cells, miR-335-5p expression is inhibited. miR-335-5p targets the 3’-UTR and decreases expression of intercellular adhesion molecule 1 (ICAM‑1) mRNA, an oncogene protein that drives the metastasis of tumour cells by recruiting inflammatory cells and promoting the proliferation, angiogenesis and invasion of cancer cells [168].

在PTC细胞中，miR-335-5p表达受到抑制。miR-335-5p靶向3'-UTR并降低细胞间粘附分子1（ICAM-1）mRNA的表达，ICAM-1是一种致癌基因蛋白，通过募集炎性细胞并促进癌细胞的增殖，血管生成和侵袭来驱动肿瘤细胞的转移[168。

Pellino-1 (PELI1), a novel cancer-related E3 ubiquitin ligase, is expressed in various cancers [169]. Loss of miR-30c-5p induces an increase in PELI1 and then activates the PI3K/AKT signalling pathway, leading to PTC cell proliferation and migration [169]..

Pellino-1（PELI1）是一种新型的癌症相关E3泛素连接酶，在各种癌症中均有表达。miR-30c-5p的缺失诱导PELI1的增加，然后激活PI3K/AKT信号通路，导致PTC细胞增殖和迁移。。

lncRNAs

lncRNAs

lncRNAs are a class of transcripts that are more than 2000 nucleotides in length that cannot be translated into proteins [170]. lncRNAs can regulate chromatin dynamics, gene expression or protein stability to modulate tumour cell growth, differentiation and development [171].

lncRNAs是一类长度超过2000个核苷酸的转录本，不能翻译成蛋白质。lncRNAs可以调节染色质动力学、基因表达或蛋白质稳定性，以调节肿瘤细胞的生长、分化和发育。

lncRNAs also participate in the generation of aggressive phenotypes of PTC. For example, the expression of the lncRNA SLC26A4-AS1 is significantly decreased in PTC, and this is associated with the increased expression of multiple DNA double-strand break (DSB) repair genes, especially genes encoding proteins in the MRE11/RAS50/NBS1 (MRN) complex [170].

lncRNA也参与PTC侵袭性表型的产生。例如，PTC中lncRNA SLC26A4-AS1的表达显着降低，这与多个DNA双链断裂（DSB）修复基因的表达增加有关，特别是编码MRE11/RAS50/NBS1（MRN）复合物中蛋白质的基因[170。

In addition, SLC26A4-AS1 can simultaneously interact with DDX5 and the E3 ligase TRIM25, thereby enhancing the degradation of DDX5 via the ubiquitin-proteasome pathway. This process enhances the ability of PTC cells to invade and metastasise [170]. HOTAIR (HOX transcript antisense intergenic RNA), a well-known lncRNA, sponges miR-1 and induces CCND2 expression or interacts with polycomb repressive complex 2 (PRC2) or lysine-specific histone demethylase 1 (LSD1) to regulate H3K27 trimethylation and H3K4 demethylation, respectively [172, 173].

此外，SLC26A4-AS1可以同时与DDX5和E3连接酶TRIM25相互作用，从而通过泛素-蛋白酶体途径增强DDX5的降解。这个过程增强了PTC细胞侵袭和转移的能力。HOTAIR（HOX转录物反义基因间RNA）是一种众所周知的lncRNA，它海绵状miR-1并诱导CCND2表达或与多梳抑制复合物2（PRC2）或赖氨酸特异性组蛋白脱甲基酶1（LSD1）相互作用以调节H3K27三甲基化和H3K4脱甲基化[172173]。

Moreover, HOTAIR can inhibit DLX1 expression via the modulation of histone modifications [174]. As a consequence, the lncRNA HOTAIR promotes the proliferation, migration and invasion of PTC..

此外，HOTAIR可以通过调节组蛋白修饰来抑制DLX1的表达。因此，lncRNA HOTAIR促进PTC的增殖，迁移和侵袭。。

circRNAs

环状RNA

circRNAs possess a closed continuous loop structure, and they are generated primarily from the back-splicing of precursor mRNAs (pre-mRNAs) and rarely from the self-splicing introns of ribosomal RNAs, mitochondrial RNAs and tRNAs; they may or may not have protein coding ability [175,176,177]. According to their origins, circRNAs can be divided into circular intronic RNAs (ciRNAs), exotic circRNAs (EciRNAs) and exon–intron circRNAs (EIciRNAs) [178].

circRNA具有闭合的连续环结构，它们主要由前体mRNA（pre-mRNA）的反向剪接产生，很少由核糖体RNA，线粒体RNA和tRNA的自剪接内含子产生；它们可能具有或不具有蛋白质编码能力[175176177]。根据其起源，circRNA可分为环状内含子RNA（ciRNA），外来circRNA（eciRNA）和外显子-内含子circRNA（eiciRNA）[178]。

Recent research indicates that circRNAs play essential roles in the regulation of tumour cells by functioning as activity regulators. They act as miRNA sponges, agents that interact with proteins, or translation templates to activate or inhibit the progression of tumour cells [175, 179]..

最近的研究表明，circRNA通过充当活性调节剂在肿瘤细胞的调节中发挥重要作用。它们充当miRNA海绵，与蛋白质相互作用的试剂或翻译模板，以激活或抑制肿瘤细胞的进展[175179]。。

In PTC, circEIF3I interacts with AU-rich element (ARE) RNA-binding factor 1 (AUF1) to increase Cyclin D1 mRNA stability and increase its translation, resulting in the promotion of PTC progression [180]. In addition, circPRKCI functions as a sponge for miR-1301-3p to modulate the expression of HMGB1, which regulates transcription and DNA organisation in the nucleus [181].

在PTC中，circEIF3I与富含AU的元件（ARE）RNA结合因子1（AUF1）相互作用，以增加细胞周期蛋白D1 mRNA的稳定性并增加其翻译，从而促进PTC进展。此外，circPRKCI作为miR-1301-3p的海绵调节HMGB1的表达，HMGB1调节细胞核中的转录和DNA组织。

Circ_0000644 sponges miR-671-5p, increasing annexin A2 (ANXA2) expression, resulting in the promotion of PTC malignancy [182]. Together, these findings indicate that noncoding RNAs are also key drivers that promote the development of aggressive and malignant behaviours in PTC..

Circ\u 0000644海绵miR-671-5p，增加膜联蛋白A2（ANXA2）的表达，导致PTC恶性肿瘤的促进（182）。。。

Tumour microenvironmentInnervationThe TME, which consists of a variety of cellular and noncellular components, is essential for the invasion and progression of PTC [175]. Both nerve density and perineural invasion are associated with the aggressiveness of PTC. The mechanism may involve proNGF/NGF, the ligand of the tyrosine kinase receptor TrkA, which stimulates nerve terminal outgrowth via the TrkA signalling pathway in the PTC microenvironment [66].Hu et al.

肿瘤微环境保护TME由多种细胞和非细胞成分组成，对PTC的侵袭和进展至关重要。神经密度和神经周围浸润都与PTC的侵袭性有关。该机制可能涉及proNGF/NGF，酪氨酸激酶受体TrkA的配体，它通过PTC微环境中的TrkA信号通路刺激神经末梢生长。胡等人。

reported that alterations in neural biological processes contribute to the formation of the PTC microenvironment [183]. In PTC tissues, different types of neurons, such as cholinergic, dopaminergic, and serotonergic neurons, classified by neuronal markers, can play modulatory roles in microenvironment formation.

。在PTC组织中，按神经元标记分类的不同类型的神经元，例如胆碱能，多巴胺能和5-羟色胺能神经元，可以在微环境形成中起调节作用。

For example, the cholinergic marker SLC18A3 is positively correlated with activated CD8+ T cells, effector memory CD8+ T cells, and T-cell trafficking, whereas the dopaminergic marker SLC6A3 and serotonergic markers show negative correlations with these T-cell changes [183] (Fig. 5).Fig. 5: Influence of the tumour microenvironment on the aggressiveness of PTC.The tumour microenvironment (TME), which consists of a variety of cellular and non-cellular components, is an essential factor in the aggressiveness of PTC.

例如，胆碱能标记物SLC18A3与活化的CD8+T细胞，效应记忆CD8+T细胞和T细胞运输呈正相关，而多巴胺能标记物SLC6A3和血清素能标记物与这些T细胞变化呈负相关[183]（图5）。图5：肿瘤微环境对PTC侵袭性的影响。肿瘤微环境（TME）由多种细胞和非细胞成分组成，是PTC侵袭性的重要因素。

Nerve density and perineural invasion modulate the TME. Cancer-associated fibroblasts (CAFs) and tumour-associated neutrophils (TANs) infiltrate in TME, which are associated with tumour cell motility, progression, proliferation and dissemination. In addition, some microelements and metabolic syndrome (MetS) are closely related to the aggressive behaviours of PTC.Full size imageCancer-associated fibroblastsCancer-associated fibroblasts (CAFs) constitute the main cell type in the tumour stroma.

神经密度和神经周围浸润调节TME。癌症相关成纤维细胞（CAF）和肿瘤相关中性粒细胞（TAN）浸润TME，这与肿瘤细胞的运动，进展，增殖和传播有关。此外，一些微量元素和代谢综合征（MetS）与PTC的攻击行为密切相关。全尺寸图像癌症相关成纤维细胞扫描相关成纤维细胞（CAF）构成肿瘤基质中的主要细胞类型。

Duri.

很难。

ReferencesDeng Y, Li H, Wang M, Li N, Tian T, Wu Y, et al. Global burden of thyroid cancer from 1990 to 2017. JAMA Netw Open. 2020;3:e208759.PubMed

参考文献Deng Y，Li H，Wang M，Li N，Tian T，Wu Y等。1990年至2017年甲状腺癌的全球负担。JAMA网络打开。2020年；3： e208759.PubMed

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Download referencesFundingThis work was supported by grants from the National Natural Science Foundation of China (82103549, 82273367), and the Excellent Youth Training Programme of the First Affiliated Hospital of Fujian Medical University (2023FY-YXQN-2).Author informationAuthors and AffiliationsDepartment of Thyroid and Breast Surgery, the First Affiliated Hospital, Fujian Medical University, Fuzhou, ChinaJunsi Zhang & Sunwang XuDepartment of Thyroid and Breast Surgery, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, ChinaSunwang XuFujian Provincial Key Laboratory of Precision Medicine for Cancer, Fuzhou, ChinaSunwang XuAuthorsJunsi ZhangView author publicationsYou can also search for this author in.

下载参考文献资助这项工作得到了国家自然科学基金（8210354982273367）和福建医科大学第一附属医院优秀青年培训计划（2023FY-YXQN-2）的资助。作者信息作者和附属机构福建医科大学附属第一医院甲状腺与乳腺外科，福州，中国张俊思和徐孙旺福建医科大学附属第一医院滨海校区国家区域医学中心甲状腺与乳腺外科，福州，中国徐孙旺福建省癌症精准医学重点实验室，福州，徐孙旺作者张俊思观点作者出版物您也可以在中搜索这位作者。

PubMed Google ScholarSunwang XuView author publicationsYou can also search for this author in

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Reprints and permissionsAbout this articleCite this articleZhang, J., Xu, S. High aggressiveness of papillary thyroid cancer: from clinical evidence to regulatory cellular networks.

转载和许可本文引用本文Zhang，J.，Xu，S。乳头状甲状腺癌的高侵袭性：从临床证据到调节细胞网络。

Cell Death Discov. 10, 378 (2024). https://doi.org/10.1038/s41420-024-02157-2Download citationReceived: 22 April 2024Revised: 20 August 2024Accepted: 21 August 2024Published: 26 August 2024DOI: https://doi.org/10.1038/s41420-024-02157-2Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

细胞死亡发现。10378（2024）。https://doi.org/10.1038/s41420-024-02157-2Download引文收到日期：2024年4月22日修订日期：2024年8月20日接受日期：2024年8月21日发布日期：2024年8月26日OI：https://doi.org/10.1038/s41420-024-02157-2Share本文与您共享以下链接的任何人都可以阅读此内容：获取可共享链接对不起，本文目前没有可共享的链接。复制到剪贴板。

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