Archives of gynecology and obstetrics · 2013
Valproic acid suppresses cervical cancer tumor progression possibly via activating Notch1 signaling and enhances receptor-targeted cancer chemotherapeutic via activating somatostatin receptor type II.
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Tsai Cheguo, Leslie Juliana S, Franko-Tobin Laura G, Prasnal Monica C, Yang Tong, Vienna Mackey L, Fuselier Joseph A, Coy David H, Liu Mingqiu, Yu Changyuan, Sun Lichun
Аннотация
PURPOSE: We investigated the effects of the anti-epilepsy drug valproic acid (VPA) alone and in combination in treating cervical cancer.
METHODS: VPA was investigated for its effects on cervical cancer Hela cell proliferation and tumor growth via in vitro and in vivo assays.
RESULTS: VPA induce cell growth suppression and cell cycle arrest, with an increase of Notch1 that acts as a tumor suppressor and the change of other tumor-associated genes such as p21, p63 and PCNA. VPA was also found to induce cell morphological change, with an increase of certain cell transformation markers such as snail1, snail2 and N-cadherin. Moreover, VPA could significantly up-regulate somatostatin receptor type II (SSTR2). Our in vivo study further demonstrated that VPA via inducing SSTR2 up-regulation extremely enhanced the anti-tumor ability of the SSTR2-preferential cytotoxic COL-SST conjugate in xenografts.
CONCLUSIONS: VPA could not only suppress tumor progression but also provide a novel promising therapeutic choice in combination with a receptor-targeted cytotoxic conjugate via activating the specific receptor.
METHODS: VPA was investigated for its effects on cervical cancer Hela cell proliferation and tumor growth via in vitro and in vivo assays.
RESULTS: VPA induce cell growth suppression and cell cycle arrest, with an increase of Notch1 that acts as a tumor suppressor and the change of other tumor-associated genes such as p21, p63 and PCNA. VPA was also found to induce cell morphological change, with an increase of certain cell transformation markers such as snail1, snail2 and N-cadherin. Moreover, VPA could significantly up-regulate somatostatin receptor type II (SSTR2). Our in vivo study further demonstrated that VPA via inducing SSTR2 up-regulation extremely enhanced the anti-tumor ability of the SSTR2-preferential cytotoxic COL-SST conjugate in xenografts.
CONCLUSIONS: VPA could not only suppress tumor progression but also provide a novel promising therapeutic choice in combination with a receptor-targeted cytotoxic conjugate via activating the specific receptor.
Предметные рубрики MeSH
AnimalsAnticonvulsantsCarcinomaCell DifferentiationCell ProliferationColchicineCyclin-Dependent Kinase Inhibitor p21Cyclooxygenase 2Drug CombinationsG2 Phase Cell Cycle CheckpointsGene ExpressionGenes, p53HeLa CellsHormonesHumansMembrane ProteinsMiceMice, NudePTEN PhosphohydrolasePhosphatidylinositol 3-KinasesRNA, MessengerReceptor, Notch1Receptors, SomatostatinSignal TransductionSomatostatinTubulin ModulatorsValproic Acid