Gap junction function and cancer.
Gap junction function and cancer.
复制标题
间隙连接功能与癌症。
作者：
Holder Jw;E. Elmore;Barrett Jc
间隙连接（GJ）提供必需代谢物和离子的细胞间通信。GJ允许组织平均反应，清除废物，并通过稀释和允许稳态催化剂来最大限度地减少外源性物质的影响。许多化学物质会对膜GJ组装产生不利影响，导致GJ细胞间通讯的可逆改变。在毒性过程中，必需代谢物、离子和调节剂在整个组织群落中不能稳态地共享。代谢回路的改变被认为会中断器官整合。持续的GJ扰动可引起慢性效应（例如，癌症），并且许多肿瘤促进剂抑制GJ细胞间通讯。肝癌前病灶在病灶边界内与正常细胞不适当地（或根本不）相互连通（但水平降低）。随着时间的推移，病灶可能变得不那么受控制，并且在组织内更加孤立。GJ在肿瘤进展阶段保持定量减少，并且在转移中可能发生定性改变，因为在原发性肿瘤细胞和继发性转移部位的外源宿主细胞之间建立了连接。细胞粘附分子和整联蛋白的细胞分选和结合机制也可能在二级位点发生改变。这可能允许原发性肿瘤细胞的重新定位和通过继发部位的GJ的养育。
Gap junctions (GJs) provide cell-to-cell communication of essential metabolites and ions. GJs allow tissues to average responses, clear waste products, and minimize the effects of xenobiotics by dilution and allowing steady-state catabolism. Many chemicals can adversely affect the membrane GJ assembly causing reversible alterations in GJ intercellular communication. During toxicity essential metabolites, ions, and regulators are not shared homeostatically throughout a tissue community. Alterations in metabolic circuits are thought to interrupt organ integration. Persistent GJ perturbation can cause chronic effects (e.g., cancer), and many tumor promoters inhibit GJ intercellular communication. Liver precancerous foci intracommunicate (but at a reduced level) and intercommunicate improperly (or not at all) across the foci boundary to normal cells. In time, foci can become less regulated and more isolated within the tissue. GJs remain reduced quantitatively in the tumor progression stage and may be qualitatively altered in metastasis since connections are made between the primary tumor cells and foreign host cells at the secondary metastatic site. Cell sorting and binding mechanisms by the cell adhesion molecules and integrins may also be altered at secondary sites. This may allow the relocation of primary tumor cells and nurturance via GJs at the secondary site.
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影响因子：
3.4
作者：
Alonso P. Moreno;A. C. C. D. Carvalho-A.-C.-C.-D.-Carvalho-2259865318;V. Verselis;B. Eghbali;David C. Spray;Z. Gatmaitan;R. L. White;A. C. C. D. Carvalho-A.-C.-C.-D.-Carvalho-2259865318
通讯作者：
Alonso P. Moreno;A. C. C. D. Carvalho-A.-C.-C.-D.-Carvalho-2259865318;V. Verselis;B. Eghbali;David C. Spray;Z. Gatmaitan;R. L. White;A. C. C. D. Carvalho-A.-C.-C.-D.-Carvalho-2259865318
新鲜分散的小鼠胰腺β细胞对之间间隙连接的生物物理特性。
影响因子：
3.4
作者：
Perez-Armendariz,M;Roy,C;Spray,DC;Bennett,MV
通讯作者：
Bennett,MV
干细胞致癌理论。
影响因子：
3.5
作者：
Trosko,JE;Chang,CC
通讯作者：
Chang,CC
DOI：
10.1002/tcm.1770100205
发表时间：
1990
期刊：
Teratogenesis, carcinogenesis, and mutagenesis
影响因子：
--
作者：
D. JamesFitzgerald;H. Yamasaki
通讯作者：
D. JamesFitzgerald;H. Yamasaki
影响因子：
11.2
作者：
Emmanuel Farber;Harry Rubin
通讯作者：
Emmanuel Farber;Harry Rubin