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. Author manuscript; available in PMC: 2016 May 18.
Published in final edited form as: Oncogene. 2015 May 18;35(7):919–928. doi: 10.1038/onc.2015.146

Figure 4. MALT1 contributes to EGFR- but not K-ras-driven lung adenocarcinoma progression.

Figure 4

(a) Graphic presentation of the generation of tetO-EGFRL858R; CCSP-rtTA; MALT1−/− triple-transgenic mice. (b) Graphic presentation of the generation of LSL-K-rasG12D; CCSP-Cre; MALT1−/− triple-transgenic mice. (c) Total RNA were extracted from the lungs of tetO-EGFRL858R; CCSP-rtTA; Malt1+/− mice (Het), tetO-EGFRL858R; CCSP-rtTA; Malt1−/− mice (KO), and HeLa cells, respectively. Reverse transcription PCR was performed using primers to amplify human EGFR and mouse LCa3, respectively. (d) The ratio of lung to body weight was compared between tetO-EGFRL858R; CCSP-rtTA; MALT1+/− (Het) (n=8) and tetO-EGFRL858R; CCSP-rtTA; MALT1−/− (KO) mice (n=7). **, p<0.01. (e) H&E staining of the normal lung (NL), lung from tetO-EGFRL858R; CCSP-rTTA; MALT1+/− mice (Het) and lung from tetO-EGFRL858R; CCSP-rTTA; MALT1−/− mice (KO). (f) The ratio of lung to body weight was compared between LSL-K-rasG12D; CCSP-Cre; MALT1+/− (Het) (n=5) and LSL-K-rasG12D; CCSP-Cre; MALT1−/− (KO) mice (n=5). ns, no statistically significance. (g) The number of tumors on the lung in LSL-K-rasG12D; CCSP-Cre; MALT1+/− (Het) (n=3) and LSL-K-rasG12D; CCSP-Cre; MALT1−/− (KO) mice (n=3). ns, no statistically significance. (h) H&E staining of the lung from LSL-K-rasG12D; CCSP-Cre; MALT1+/− mice (Het) and lung from LSL-K-rasG12D; CCSP-Cre; MALT1−/− mice (KO). Arrow shows tumor cells.