PITX2 promotes ovarian cancer cell growth.

<p>(<b>A</b>) PITX2A stable expressing clones were established in SKOV3 and OVCA433 cells. Western blot analysis using anti-HA antibody showed the expression levels of HA-tagged PITX2A in C4 and C5 clones of SKOV-3, and C33 and C34 clones of OVCA 433. β-actin was used as loading control. (<b>B</b>) Western blot analysis using anti-PITX2 antibody showed the reduced expressions of endogenous PITX2 in stable knockdown clones generated by 2 shRNA constructs (K1 and K2). Scrambled is the non-specific shRNA control. The numerical units represent the relative expressions of PITX2 reduction in each stable clone as compared with the scrambled controls. β-actin was used as loading control. (<b>C</b>) Ectopic expression of PITX2A stimulated cell proliferation in ovarian cancer cells. Both C4 and C5 of SKOV-3 cells demonstrated 1.5- fold increase of cell growth (* <i>P</i><0.05), C33 and C34 of OVCA 433 cells had 3- fold increase of cell growth (** <i>P</i><0.01) as compared with their vector control. (<b>D</b>) Depletion of endogenous PITX2 reduced cell proliferation in ovarian cancer cells. A 3- to 4- fold of reduction on cell viability in both knockdown clones (K1 and K2) of OV2008 cells (** <i>P</i><0.01) and 2- to 3- fold decrease on cell proliferation in knockdown clones (K1 and K2) of OVCA 433 cells (* <i>P</i><0.05) were observed.