Key result
Angiotensin-(1-7) significantly suppressed VEGFa expression, tumor-associated angiogenesis, and tumor growth in acquired platinum-resistant non-small cell lung cancer models.
Why the study?
The study was designed to investigate the effect of Ang-(1-7) on tumor-associated angiogenesis in DDP-resistant lung cancer cell lines.
Does Ang-(1-7) reduce tumor-associated angiogenesis in DDP-resistant non-small cell lung cancer models?
Does Ang-(1-7) reduce tumor-associated angiogenesis in DDP-resistant non-small cell lung cancer models?
Ang-(1-7) suppresses tumor-associated angiogenesis in platinum-resistant non-small cell lung cancer models via PI3K/AKT and MAPK pathways.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications in lung cancer; hypothesis-generating for Ang-(1-7) antiangiogenic effects.
Renin-angiotensin system (RAS) signaling has been implicated in the development of cancer. The new RAS ACE2/Ang-(1-7)/Mas axis antagonizes the classical ACE/Ang II/AT1R axis. Ang-(1-7) has pleiotropic roles in lung cancer including suppressing proliferation, angiogenesis, and metastasis. This research was designed to investigate the effect of Ang-(1-7) on tumor-associated angiogenesis in DDP-resistant lung cancer cell lines. We first established acquired DDP-resistant cell lines A549 (A549-DDP) and LLC (LLC-DDP). We next performed RT-qPCR, western blot, ELISA, tube formation, microvessel density detection, immunohistochemistry, and tumor formation assays. The results showed that the mRNA and protein levels of RAS components and vascular endothelial growth factor A (VEGFa) were lessened in the A549/LLC-DDP+Ang-(1-7) group compared with the A549/LLC-DDP group. This effect could be blocked by the MAS receptor antagonist A779. The data revealed that Ang-(1-7) could perform its antiangiogenic function by PI3K/AKT and MAPK pathways. Furthermore, the impact of Ang-(1-7) on tumor-associated angiogenesis has been confirmed in lung cancer xenograft model with acquired DDP resistance. These results provide a theoretical basis for designing therapeutic strategies for targeting Ang-(1-7) in the treatment of NSCLC.
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Geng et al. (2021) studied Non-small cell lung cancer (NSCLC) with acquired platinum resistance (n=18). Angiotensin-(1-7) vs. Vehicle/Control (A549-DDP) or Ang-(1-7) + A779 was evaluated on Tumor growth, VEGFa expression, and angiogenesis (microvessel density) (p=<0.05). Angiotensin-(1-7) significantly suppressed VEGFa expression, tumor-associated angiogenesis, and tumor growth in acquired platinum-resistant non-small cell lung cancer models.
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