Endostatin improves cancer-associated systemic syndrome in a lung cancer model

Wang, Xia; Zhan, Rui‐Yu; Wang, Yu‐Yi; Xi, Yan; Cao, Dan; Li, Yan; Luo, Feng

doi:10.3892/ol.2015.3049

Cited by 1 publication

(1 citation statement)

References 22 publications

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“…although there are a number of studies about endostatin inhibiting MM tumor microvessels, it remains unclear whether it can inhibit MM growth by regulating the polarity of macrophages. Some studies have found that endostatin enhanced the anti-tumor immune response and increased the infiltration of cytotoxic T lymphocytes to the TMe and polarized the macrophages that reached the tumor tissue to M1-type, resulting in an increased proportion of M1-type TaMs and reduced proportion of M2-type TaMs, thereby reversing the immunosuppressive environment in the TMe (8,(29)(30)(31). From the perspective of the change of macrophage polarity, the present study briefly explored that the inhibition of endostatin on B16 cells may be partly due to its immunological function, but the specific mechanism requires further study.…”

Section: Discussionmentioning

confidence: 99%

Endostatin inhibits the proliferation and migration of B16 cells by inducing macrophage polarity to M1‑type

et al. 2021

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Malignant melanoma is a common skin tumor that easily metastasizes and has a poor prognosis. endostatin is an endogenous vascular endothelial inhibitor that mainly suppresses tumor growth by inhibiting the proliferation of vascular endothelial cells and by reducing the formation of tumor microvessels, however the immunological function of endostatin remains unclear. Previously, we have found that an over-expression endostatin (pendostatin) plasmid induced raW264.7 cells' polarity to M1-type macrophage. To elucidate the effect of M1-type macrophages induced by endostatin on melanoma B16 cells, the present study transfected raW264.7 cells with pendostatin plasmid and co-cultured them with B16 cells. compared with the control group, the expression of matrix metalloproteinase (MMP)-2, MMP-9 and proliferating cell nuclear antigen in B16 cells was inhibited by M1-type macrophages, but cleaved caspase-3 and cleaved caspase-8 were significantly upregulated and the ratio of Bax/Bcl-2 was increased. These results indicated that M1 macrophages induced by pendostatin plasmid inhibited the proliferation and migration of B16 cells and promoted their apoptosis. These findings suggest that the inhibitory effect of endostatin on melanoma is not limited to directly inhibiting tumor microvessel formation, but it may also be related to regulating changes in macrophage polarity.

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Section: Discussionmentioning

confidence: 99%