HSPA12B: a novel facilitator of lung tumor growth
He Ma, Ting Lu, Xiaojin Zhang, Chuanfu Li, Jingwei Xiong, Lei Huang, Ping Liu, Yuehua Li, Li Liu, Zhengnian Ding
TL;DR
This study shows that HSPA12B promotes lung tumor growth through a Cox-2-dependent mechanism, suggesting it could be a new target for lung cancer treatment.
Contribution
The study identifies HSPA12B as a novel facilitator of lung tumor growth and a potential therapeutic target.
Findings
Transgenic mice overexpressing HSPA12B developed more and larger lung tumors compared to wild-type mice.
HSPA12B-induced tumor growth was suppressed by the Cox-2 inhibitor celecoxib, reducing angiogenesis and proliferation.
Celecoxib reversed HSPA12B-induced changes in angiopoietin-1, eNOS phosphorylation, and AKAP12 levels.
Abstract
Lung tumor progression is regulated by proangiogenic factors. Heat shock protein A12B (HSPA12B) is a recently identified regulator of expression of proangiogenic factors. However, whether HSPA12B plays a role in lung tumor growth is unknown. To address this question, transgenic mice overexpressing HSPA12B (Tg) and wild-type littermates (WT) were implanted with Lewis lung cancer cells to induce lung tumorigenesis. Tg mice showed significantly higher number and bigger size of tumors than WT mice. Tg tumors exhibited increased angiogenesis and proliferation while reduced apoptosis compared with WT tumors. Interestingly, a significantly enhanced upregulation of Cox-2 was detected in Tg tumors than in WT tumors. Also, Tg tumors demonstrated upregulation of VEGF and angiopoietin-1, downregulation of AKAP12, and increased eNOS phosphorylation compared with WT tumors. Celecoxib, a selective…
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Taxonomy
TopicsAncient Egypt and Archaeology · Ancient Mediterranean Archaeology and History · Archaeology and Historical Studies