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. 2017 Nov 6;37(8):1086–1094. doi: 10.1038/onc.2017.383

Figure 2.

Figure 2

DHRS2 suppressed tumor cell growth in vitro and in vivo. (a) The relative quantification of DHRS2-V1 and DHRS2-V2 in transfected KYSE30 and KYSE510 cells compared with vector control cells (-Vec) respectively (**P<0.01). (b, c) Foci formation assay (b) and soft agar assay (c) demonstrated that DHRS2-V1 and DHRS2-V2 inhibited the anchorage-dependent and -independent cell growth ability. The results were summarized as mean±s.e.m. of three independent assays (**P<0.01). (d) The DHRS2 RNA level decreased in DHRS2 knock-down KYSE180 and HKESC1 (shRNA) cells compared with vector control (c) cells (*P<0.05; **P<0.01). (e) Cell proliferation increased in DHRS2 knock-down cells compared with control cells (*P<0.05). (f) Foci formation ability increased in DHRS2 knock-down cells compared with control cells. (g) The representative pictures of xenografts formed in nude nice (n=6). Tumor volume and tumor weight significantly decreased in DHRS2-V1 and DHRS2-V2-transfected KYSE30 cells (**P<0.01). (h) The representative pictures of DHRS2 staining of xenograft sections (original magnification: × 200).