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碳酸酐酶 XII 的表达在上皮间质转化过程中受到调节，并通过蛋白激酶 C 信号通路进行调控。

Carbonic Anhydrase XII Expression Is Modulated during Epithelial Mesenchymal Transition and Regulated through Protein Kinase C Signaling.

机构信息

Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy.

Laboratory of Clinical Proteomics, "Giovanni Paolo II" Hospital, 73100 ASL-Lecce, Italy.

出版信息

Int J Mol Sci. 2020 Jan 22;21(3):715. doi: 10.3390/ijms21030715.

DOI:10.3390/ijms21030715
PMID:31979064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7037142/
Abstract

Members of the carbonic anhydrase family are functionally involved in the regulation of intracellular and extracellular pH in physiological and pathological conditions. Their expression is finely regulated to maintain a strict control on cellular homeostasis, and it is dependent on the activation of extracellular and intracellular signaling pathways. Combining RNA sequencing (RNA-seq), NanoString, and bioinformatics data, we demonstrated that the expression of carbonic anhydrase 12 (CAXII) is significantly different in luminal and triple negative breast cancer (BC) models and patients, and is associated with the activation of an epithelial mesenchymal transition (EMT) program. In BC models, the phorbol ester 12-myristate 13-acetate (PMA)-mediated activation of protein kinase C (PKC) induced a down-regulation of CAXII with a concomitant modulation of other members of the transport metabolon, including CAIX and the sodium bicarbonate cotransporter 3 (NBCn1). This is associated with a remodeling of tumor glycolytic metabolism induced after PKC activation. Overall, this analysis highlights the dynamic nature of transport metabolom and identifies signaling pathways finely regulating this plasticity.

摘要

碳酸酐酶家族的成员在生理和病理条件下参与细胞内和细胞外 pH 值的调节。它们的表达受到精细调节，以维持细胞内环境的严格控制，并且依赖于细胞外和细胞内信号通路的激活。通过 RNA 测序 (RNA-seq)、NanoString 和生物信息学数据分析，我们证明碳酸酐酶 12 (CAXII) 的表达在腔型和三阴性乳腺癌 (BC) 模型和患者中存在显著差异，并与上皮间质转化 (EMT) 程序的激活相关。在 BC 模型中，佛波酯 12-肉豆蔻酸 13-乙酸酯 (PMA) 介导的蛋白激酶 C (PKC) 的激活导致 CAXII 的下调，同时还调节了其他转运代谢物的成员，包括 CAIX 和碳酸氢钠共转运蛋白 3 (NBCn1)。这与 PKC 激活后诱导的肿瘤糖酵解代谢的重塑有关。总的来说，这项分析强调了转运代谢组的动态性质，并确定了精细调节这种可塑性的信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ae4/7037142/4e0715ac0352/ijms-21-00715-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ae4/7037142/4e0715ac0352/ijms-21-00715-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ae4/7037142/1fe5050d7b19/ijms-21-00715-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ae4/7037142/0de1358193e7/ijms-21-00715-g003.jpg
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