CAJ | 학술논문

转化生长因子-β受体(TpR)Ⅲ在多种肿瘤组织中常表达缺失,并能负性调控肿瘤的发生,其机制除了依赖Smads的典型转化生长因子-β(TGF-β)信号通路外,还能通过影响P38丝裂原活化蛋白激酶(MAPK)、转录核因子-κB (NF-κB)、Cdc42以及产生可溶性TβR(sTβR)Ⅲ等多种机制调控肿瘤的侵袭、迁移、增殖和凋亡.进一步明确TβRⅢ在肿瘤组织中表达缺失的机制对肿瘤的诊断、治疗和预后评估意义重大.
전화생장인자-β수체(TpR)Ⅲ재다충종류조직중상표체결실,병능부성조공종류적발생,기궤제제료의뢰Smads적전형전화생장인자-β(TGF-β)신호통로외,환능통과영향P38사렬원활화단백격매(MAPK)、전록핵인자-κB (NF-κB)、Cdc42이급산생가용성TβR(sTβR)Ⅲ등다충궤제조공종류적침습、천이、증식화조망.진일보명학TβRⅢ재종류조직중표체결실적궤제대종류적진단、치료화예후평고의의중대.
The expression of transforming growth factor(TGF)-β supeffamily co-receptor (Tβ3R) Ⅲ is often lost in many kinds of cancers.Tβ3RⅢ plays a role of negative regulation in tumorigenesis.T3RⅢ could regulate the cellular invasion,migration,proliferation and apoptosis by multiple mechanisms,such as mediating the TGF-β signaling pathway,impacting the mitogen-activated protein kinase(MAPK),nuclear factor-kappa B (NF-κB) and Cdc42 and producing soluble TβR(sTβR) Ⅲ.Defining the mechanisms of absence and physiological functions of TβR Ⅲ in cancers has great significant for the diagnosis,treatment and prognosis of cancer.