Skip to main content
Fig. 3 | BMC Cancer

Fig. 3

From: Semaphorin 3A mediated brain tumor stem cell proliferation and invasion in EGFRviii mutant gliomas

Fig. 3

Sema3A mediates antiproliferative effects via Nrp1 and PlxnA1. a Quantitation of proliferation assay comparing mean DAPI labeled cells per field in Control, Nrp1-KD, and PlxnA1-KD infected BTSCs in the absence and presence of Sema3A (10 ng/mL). Control non-targeting virus treated cells maintain the antiproliferative response to Sema3A. Nrp1-KD and PlxnA1-KD BTSCs demonstrate a decreased baseline proliferation, and show no difference between untreated and treated conditions. b Quantitation of the mean change in DAPI labeled cells per field over 24 h. In control non-targeting virus treated BTSCs, Sema3A abolishes proliferation, as there is no change in cell number between the start and end of the assay. Similarly, there is no change in Nrp1-KD BTSC proliferation in untreated or treated conditions. Here, the proliferation rate of PlxnA1-KD BTSCs was not significantly different than non-targeting virus treated BTSCs but showed loss of the Sema3A antiproliferative response (***p < 0.0005; NS, not significant)

Back to article page
\