Endostar enhances anti-tumor effects of radiation via inhibition of HIF-1α and bFGF in lung adenocarcinoma cell line A549

Xu, Huilin; Ge, Wei; Jie, Fangfang; Cao, Dedong; Ming, Pingpo; Luo, Wei; Jiang, Song; Li, Changhu

doi:10.1007/s10330-013-1255-2

Cited by 2 publications

(2 citation statements)

References 15 publications

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“…With this inhibitor, ear hole closure is totally blocked. This is consistent with previously reported observations that endostatin suppresses HIF-1a expression (20,21) as we show in this study, although other reports do suggest that endostatin is HIF-independent (22). This is in contrast to studies showing that endostatin treatment of different types of cutaneous skin wounds leaves the wound repair process unaffected or even enhanced by endostatin treatment with reduced hypertrophic scar formation (23)(24)(25)(26).…”

Section: Introductionsupporting

confidence: 94%

“…The first phenotypic group includes three molecules, HIF-1a, CD31, and OCT3/4, which are inhibited equally by siHif and endostatin. HIF-1a has been previously shown to be down-regulated by endostatin (19)(20)(21) so that many of the inhibitory results could be due to inhibition of HIF-1a or by other endostatinspecific interactions. CD31 is a HIF-1a target and is expressed by endothelial cells, blood vessels, and cells migrating from the bone marrow.…”

Section: Neovascularizationmentioning

confidence: 99%

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Neovascularization and the recruitment of CD31+ cells from the bone marrow are unique under regenerative but not wound repair conditions

Bedelbaevak

Zhang

Azlanukov

et al. 2022

Preprint

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The long-noted observation that endostatin is a potent inhibitor of tumor vasculature but has little or no effect on wound repair or pregnancy remains an 'as of yet unexplained but remarkable phenomenon'(1). However, there is another path to wound healing, epimorphic regeneration, and here we present data in mice demonstrating that endostatin is, in fact, a potent inhibitor of epimorphic regeneration. In this study, we show that a regenerative response seen in the spontaneously regenerating MRL mouse involves CD31+ endothelial precursors that migrate from the bone marrow into the wound site and form new vessels, unlike that seen in the non-regenerating C57BL/6 mouse injury site. Furthermore, this appears to relate to the induction of HIF-1a, an inducer of regeneration (2). Inducing epimorphic regeneration in otherwise non-regenerating mice via an enhanced HIF-1a response by employing the PHD inhibitor 1,4-DPCA/hydrogel, a HIF-1a stabilizer, results in the same increased bone marrow-derived CD31+ endothelial precursor response and increased vasculogenesis. This regenerative response is completely blocked by endostatin, supporting the notion that vascularization induced during regeneration shares similarities to the tumor vasculature.

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