TGFβ signaling networks in ovarian cancer progression and plasticity.

TGFβ signaling networks in ovarian cancer progression and plasticity.
复制标题

DOI:
10.1007/s10585-021-10077-z
复制
发表时间:
2021-04
影响因子:
4
通讯作者:
Mythreye K
Mythreye K
中科院分区:
医学3区
文献类型:
--
作者:
Kumari A;Shonibare Z;Monavarian M;Arend RC;Lee NY;Inman GJ;Mythreye K

文献摘要

参考文献

被引文献

相似文献

上皮性卵巢癌(EOC)是女性癌症相关死亡的主要原因。晚期诊断有显著的肿瘤负荷,伴有复发和化疗耐药,导致这种不良预后。已知这些发病率与癌症中上皮-间质转化(EMT)相关的事件有关。在EMT期间,局部肿瘤细胞改变其极性、细胞-细胞连接、细胞-基质相互作用,获得运动性和侵袭性以及过度的转移扩散潜力。EMT的关键触发因素包括转化生长因子-β(TGFβ)家族的生长因子,其由特定肿瘤和转移环境中的多种细胞类型积极产生。虽然TGFβ可以在癌症中充当肿瘤抑制剂或促进剂,但TGFβ至少部分地通过EMT表现出其促肿瘤发生功能。如本文所述,TGFβ在转录和转录后水平调节EMT。尽管最近在基于TGFβ的治疗方面取得了进展,但对于非常需要新治疗策略的卵巢癌,进展有限。在这里,我们总结和讨论了最近的一些见解,在EMT中的TGFβ亚型的信号转导机制,在独特的转移环境中的EOCs和目前的治疗干预措施,可能是相关的。
Epithelial ovarian cancer (EOC) is a leading cause of cancer-related death in women. Late-stage diagnosis with significant tumor burden, accompanied by recurrence and chemotherapy resistance, contributes to this poor prognosis. These morbidities are known to be tied to events associated with epithelial-mesenchymal transition (EMT) in cancer. During EMT, localized tumor cells alter their polarity, cell–cell junctions, cell–matrix interactions, acquire motility and invasiveness and an exaggerated potential for metastatic spread. Key triggers for EMT include the Transforming Growth Factor-β (TGFβ) family of growth factors which are actively produced by a wide array of cell types within a specific tumor and metastatic environment. Although TGFβ can act as either a tumor suppressor or promoter in cancer, TGFβ exhibits its pro-tumorigenic functions at least in part via EMT. TGFβ regulates EMT both at the transcriptional and post-transcriptional levels as outlined here. Despite recent advances in TGFβ based therapeutics, limited progress has been seen for ovarian cancers that are in much need of new therapeutic strategies. Here, we summarize and discuss several recent insights into the underlying signaling mechanisms of the TGFβ isoforms in EMT in the unique metastatic environment of EOCs and the current therapeutic interventions that may be relevant.
DOI: 10.1002/path.2696
发表时间: 2010-05
影响因子: 7.3
作者:
Ahmed, Ashour Ahmed;Etemadmoghadam, Dariush;Temple, Jillian;Lynch, Andy G.;Riad, Mohamed;Sharma, Raghwa;Stewart, Colin;Fereday, Sian;Caldas, Carlos;DeFazio, Anna;Bowtell, David;Brenton, James D.
通讯作者: Brenton, James D.
EMT亚型影响上皮可塑性和细胞迁移模式。
DOI: 10.1016/j.devcel.2018.05.027
发表时间: 2018-06-18
期刊: Developmental cell
影响因子: 11.8
作者:
Aiello NM;Maddipati R;Norgard RJ;Balli D;Li J;Yuan S;Yamazoe T;Black T;Sahmoud A;Furth EE;Bar-Sagi D;Stanger BZ
通讯作者: Stanger BZ
染色体不稳定性通过胞质DNA反应驱动转移。
DOI: 10.1038/nature25432
发表时间: 2018-01-25
期刊: Nature
影响因子: 64.8
作者:
Bakhoum SF;Ngo B;Laughney AM;Cavallo JA;Murphy CJ;Ly P;Shah P;Sriram RK;Watkins TBK;Taunk NK;Duran M;Pauli C;Shaw C;Chadalavada K;Rajasekhar VK;Genovese G;Venkatesan S;Birkbak NJ;McGranahan N;Lundquist M;LaPlant Q;Healey JH;Elemento O;Chung CH;Lee NY;Imielenski M;Nanjangud G;Pe'er D;Cleveland DW;Powell SN;Lammerding J;Swanton C;Cantley LC
通讯作者: Cantley LC
DOI: 10.1093/annonc/mdx449
发表时间: 2017-11-01
期刊: ANNALS OF ONCOLOGY
影响因子: 50.5
作者:
Bookman, M. A.;Okamoto, A.;Ochiai, K.
通讯作者: Ochiai, K.
DOI: 10.1101/gad.2060811
发表时间: 2011-06-15
影响因子: 10.5
作者:
Aragon, Eric;Goerner, Nina;Macias, Maria J.
通讯作者: Macias, Maria J.