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. 2007 Oct 18;99(1):62–70. doi: 10.1111/j.1349-7006.2007.00635.x

Figure 1.

Figure 1

Kinesin family member 2C (KIF2C)/mitotic centromere‐associated kinesin (MCAK) overexpression in breast cancer cells. (a) Expression of KIF2C/MCAK in 14 microdissected breast cancer cases (102T, 247T, 252T, 255T, 302T, 473T, 478T, 502T, 508T, 552T, 646T, 769T, 779T, and 780T) and normal human tissues (mammary gland, lung, heart, liver, kidney, and bone marrow) by semiquantitative reverse transcription–polymerase chain reaction. β2‐Microgloblin (β2MG) served as a loading control. BM, bone marrow; MG, mammary gland. (b) Northern blot analysis of the KIF2C/MCAK transcript in eight breast cancer cell lines (HBC4, HBC5, HCC1937, MCF‐7, MDA‐MB‐231, MDA‐MB‐435S, SK‐BR‐3, and T47D) and normal human tissues, including breast, lung, heart, liver, and kidney. MUT, p53 mutant cell line; WT, p53 wild‐type cell line. A high‐intensity band was observed in breast cancer cell lines, but no signal was seen in normal tissues. β‐Actin was served as a loading control. (c) Northern blot analysis of the KIF2C/MCAK transcript in various normal human tissues. A band was observed specifically in the testis. PBL, peripheral blood leukocyte. β‐Actin served as a loading control.