Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

[Q]: To explore the antitumoral effect of indirubin on androgen-independent prostate cancer PC-3 cells and its possible mechanisms.', 'We measured the inhibitory effect of indirubin on the proliferation of prostate cancer PC-3 cells using MTT assay, detected their cell cycles by flow cytometry, and determined the expressions of the cell cycle regulatory protein cyclin D1 and its related downstream gene c-myc by Western blot.', 'The viability of the PC-3 cells was significantly decreased by indirubin in a concentration-dependent manner, reduced to 52. 2% and 13. 6% at 5 and 10 µmol/L, respectively. The cell cycle of the PC-3 cells was markedly inhibited by indirubin at 5 µmol/L, with the cells remarkably increased in the G0 and G1 phases and decreased in the S and G2/M phases. Meanwhile, indirubin also inhibited the expressions of cyclin D1 and c-myc in the Wnt signaling pathway.
[A]: Does [ Indirubin inhibit the proliferation of prostate cancer PC-3 cells ]?


[Q]: Vitamin D is associated with a number of inflammatory diseases and plays a significant role in regulating bone metabolism. Serum calcifediol was demonstrated to be potentially associated with periodontal disease. The purpose of this study was to evaluate whether an association exists between plasma calcifediol concentrations and aggressive periodontitis (AgP) and whether plasma levels of bone-related biomarkers (osteocalcin, alkaline phosphatase, calcium, and phosphorus) regulated by vitamin D are related to AgP.', 'Sixty-six patients with generalized AgP, 52 patients with chronic periodontitis, and 60 healthy controls were included in this study. Periodontal examination consisted of probing depth, attachment loss, and bleeding index measurements. Hematic calcifediol and bone-related biomarker levels were detected using radioimmunity assay kits or a biochemical analyzer.', 'Plasma calcifediol levels in patients with AgP were higher than those of healthy controls (29.28 versus 21.60 nmol/l; P <0.05) and were statistically significantly correlated with bleeding index (r = 0.321; P <0.05). Plasma osteocalcin concentrations in patients with AgP were higher than those of healthy controls (0.90 versus 0.70 ng/ml; P <0.05). Serum inorganic phosphorus values of both periodontitis groups were lower than those of healthy controls (1.06 +/- 0.18 mmol/l and 1.10 +/- 0.15 mmol/l versus 1.26 +/- 0.17 mmol/l; P <0.05).
[A]: Is elevated plasma calcifediol associated with aggressive periodontitis?


[Q]: Non-muscle myosin II (NM II) regulates a wide range of cellular functions, including neuronal differentiation, which requires precise spatio-temporal activation of Rho GTPases. The molecular mechanism underlying the NM II-mediated activation of Rho GTPases is poorly understood. The present study explored the possibility that NM II regulates neuronal differentiation, particularly morphological changes in growth cones and the distal axon, through guanine nucleotide exchange factors (GEFs) of the Dbl family.', 'NM II colocalized with GEFs, such as βPIX, kalirin and intersectin, in growth cones. Inactivation of NM II by blebbistatin (BBS) led to the increased formation of short and thick filopodial actin structures at the periphery of growth cones. In line with these observations, FRET analysis revealed enhanced Cdc42 activity in BBS-treated growth cones. BBS treatment also induced aberrant targeting of various GEFs to the distal axon where GEFs were seldom observed under physiological conditions. As a result, numerous protrusions and branches were generated on the shaft of the distal axon. The disruption of the NM II-GEF interactions by overexpression of the DH domains of βPIX or Tiam1, or by βPIX depletion with specific siRNAs inhibited growth cone formation and induced slender axons concomitant with multiple branches in cultured hippocampal neurons. Finally, stimulation with nerve growth factor induced transient dissociation of the NM II-GEF complex, which was closely correlated with the kinetics of Cdc42 and Rac1 activation.
[A]:
Does non-muscle myosin II regulate neuronal actin dynamics by interacting with guanine nucleotide exchange factors?