Fig. 4: Lap2α acts intrinsically in promoting mammary gland tumor progression.
From: LAP2α drives breast tumorigenesis by mitigating replication stress
A Tumor onset date of Lap2αflox/flox and Lap2αflox/flox;MMTV-Cre mice. Each point represents an individual animal (n = 24; n = 34). B Mammary gland tumor growth of Lap2αflox/flox or Lap2αflox/flox;MMTV-Cre mice (n = 8). Tumor size was monitored and shown. C Kaplan–Meier overall survival analysis of Lap2αflox/flox and Lap2αflox/flox;MMTV-Cre mice bearing PyMT tumors (n = 8). D IHC analysis of Lap2α, Ki-67 and γH2AX in PyMT-tumors from Lap2αflox/flox and Lap2αflox/flox;MMTV-Cre mice. Representative images are shown. E The expression level of Lap2α, Ki-67, and γH2AX from IHC stainings was scored according to the staining intensity and extent (n = 6). F ssDNA-pull down assays with nuclear extracts of PyMT-tumor cells from Lap2αflox/flox or Lap2αflox/flox;MMTV-Cre mice. G Immunostaining and confocal microscopy analysis of γH2AX foci formation in PyMT-tumor cells from Lap2αflox/flox or Lap2αflox/flox;MMTV-Cre mice under HU (2 mM, 8 h), APH (0.5 M, 8 h), or 2 h post-IR (4 Gy) treatment (n > 100 from two independent experiments). H DNA fiber assay with PyMT-tumor cells of Lap2αflox/flox or Lap2αflox/flox;MMTV-Cre mice. Cells were labeled with IdU and CldU for the indicated time followed by HU treatment in the absence or presence of MRE11 inhibitor. The ratios of CldU and IdU length were calculated in each treatment (n > 100 from two independent experiments). Data are mean ± SDs for (A), (B), (E), (G) and (H); Statistical tests were performed by Welch’s t test (A, E), two-way ANOVA with Tukey’s multiple comparisons test (B), log-rank test (C) and Kruskal–Wallis test with Dunn’s multiple comparisons test (G) and (H). Scale bar: 100 m for (D) and 10 m for (G) and (H).
