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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Biochim Biophys Acta. 2014 Nov 18;1852(1):166–174. doi: 10.1016/j.bbadis.2014.11.013

Figure 3. MALAT1 promoted CRC tumor growth in vivo.

Figure 3

SW480 cells with scramble RNA (Ctrl), stable overexpression of MALAT1 (RNAa-MALAT), or MALAT1 knockdown (RNAi-MALAT1) were injected subcutaneously into nude mice. Tumors were allowed to grow for 30 days. (A) External whole-body images, MALAT1 expression in 30 day-old tumors, and quantification of the tumor sizes. Tumors derived from RNAa-MALAT1 cells grew significantly faster than that from control cells. *P<0.05 compared to the control groups in each time point. **P<0.01 compared to the control group at 30 day after injection (n=6). (B) Representative H&E images and immunohistochemical Ki-67 staining of tumor tissues derived from control (Ctrl) or MALAT1- overexpressed cells (RNAa-MALAT1). (C) Tumor of the RNAi-MALAT1 cells grew much slower than that of control cells. *P<0.05 compared to MALAT1 knockdown group (RNAi-MALAT1). **P<0.01 compared to the control group at 30 day after injection (n=6). (D) Representative H&E images and immunohistochemical Ki-67 staining of tumor tissues derived from control (Ctrl) or MALAT1-blocked (RNAi-MALAT1) cells. RNAa-mediated MALAT1 overexpression stimulated while MALAT1 knockdown inhibited CRC cell proliferation in vivo.