Figure 5.
GOLM1 promotes tumor growth in vitro and in vivo. (A-B) The anchorage-independent growth of ALCL cells. Cells were subjected to soft agar colony formation assay individually. The colonies were stained by crystal violet and counted by using Image J software. Data from triplicate experiments were presented as mean ± SD (∗P < .05, ∗∗∗P < .001, two-tailed Student t test). (C-D) GOLM1 contributes to ALCL tumor growth in a xenograft mouse model. The tumor burden of NOD/SCID mice intraperitoneally engrafted with 2 × 107 SUP-M2-luc cells with stably expressing GOLM1, GOLM1 knockdown, or scramble control at weeks 0 and 6 were analyzed by the intensity of bioluminescence signal. Data, presented as individual mice, are representative of 3 independent experiments. NOD, nonobese diabetic; SCID, severe combined immunodeficiency; SD, standard deviation.

GOLM1 promotes tumor growth in vitro and in vivo. (A-B) The anchorage-independent growth of ALCL cells. Cells were subjected to soft agar colony formation assay individually. The colonies were stained by crystal violet and counted by using Image J software. Data from triplicate experiments were presented as mean ± SD (∗P < .05, ∗∗∗P < .001, two-tailed Student t test). (C-D) GOLM1 contributes to ALCL tumor growth in a xenograft mouse model. The tumor burden of NOD/SCID mice intraperitoneally engrafted with 2 × 107 SUP-M2-luc cells with stably expressing GOLM1, GOLM1 knockdown, or scramble control at weeks 0 and 6 were analyzed by the intensity of bioluminescence signal. Data, presented as individual mice, are representative of 3 independent experiments. NOD, nonobese diabetic; SCID, severe combined immunodeficiency; SD, standard deviation.

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