Fig. 2: Tumor cell-autonomous growth deficit through CTSD deletion. | Nature Communications

Fig. 2: Tumor cell-autonomous growth deficit through CTSD deletion.

From: Cathepsin D deficiency in mammary epithelium transiently stalls breast cancer by interference with mTORC1 signaling

Fig. 2

a Flow cytometry-based monitoring of cre recombination reporter expression (Tomato: non-recombined, GFP: recombined) in rtTA-tTS;tetO-cre;Ctsdfl/fl;mTmG PyMT cells treated for 0–4 days with doxycycline (Dox) (n = 3 independent experiments). b Analysis of CTSD expression by Western blot (with TUBA as loading control) in lysates from cells used in a. Pro/SC, zymogen/single-chain form; HC, heavy chain; LC, light chain. In vitro competitive growth assay of non-recombined and recombined rtTA-tTS;tetO-cre;Ctsdfl/fl;mTmG PyMT cells in 10% FCS (c) or 1% FCS (d) medium after a one-day pulse of Dox (n = 3 independent experiments for d 0 and d 1 in c and d 28 in d, n = 4 independent experiments for the rest). e In vivo competitive growth assay of non-recombined and recombined 10% FCS rtTA-tTS;tetO-cre;Ctsdfl/fl;mTmG PyMT cells. A one-day Dox-pulsed cell suspension of known ratio of non-recombined to recombined cells (left bar) was orthotopically transplanted into 6 recipient mice. The ratio was again determined by flow cytometry in the outgrown tumors (right bar) (n = 6 animals; two-sided one-sample t-test). Line and bar charts show all data points with mean ± SD and p-value. Source data are provided as a Source Data file.

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