Objective To investigate the effect of vascular endothelial growth factor C (VEGF-C) on apoptosis of pancreatic cancer cell. Methods Human pancreatic cancer cell line PANC-1 orthotopic implantation tumor model was established in nude mice. Primary pancreatic cancer cells and that derived from lymphatic metastasis were primarily cultured. Expression of VEGF-C was inhibited through antisense oligodeoxynucleotide in vitro transfection. Reverse transcription polynlerase chain reaction (RT-PCR) and flow cytometer were used to detect the effect of VEGF-C on apoptosis of pancreatic cancer cells and bcl-2. Results After in vitro transfection, mRNA expression level of VEGF-C in PANC-1 pancreatic cancer cells significantly decreased (P ＜0. 01 ). Apoptosis rate of pancreatic cancer cells derived from spontaneous lymphatic metastasis was (2. 83 ± 1.01 ) %, ( 4. 98 ± 2. 05 ) %,and ( 13.22 ±2. 17) % respectively for control group, SODN group and ASODN group after in vitro transfection among which apoptosis rate in ASODN group increased significantly (P ＜0. 01 ). However, apoptosis rate for pancreatic cancer cells derived from primary tumor had no obvious change (P ＞0.05), with (3.51 ±1.38)%, (4.76 ±2. 16 ) %, and (5. 33 ± 2. 18 ) % respectively in control group, SODN group and ASODN group. The expression level of bcl-2 in pancreatic cancer cells derived from spontaneous lymphatic metastasis decreased significantly (P ＜0. 05) while it had no obvious change in primary pancreatic cancer cells (P ＞ 0. 05). Conclusion To inhibit expression of VEGF-C in pancreatic cancer cell can promote apoptosis of pancreatic cancer cell, which is relevant to downregulation of bcl-2;however, it has no obvious effect on primary pancreatic cancer.

Objective To evaluate the changes in the expression of Piezo2 in spinal cord neurons in a rat model of bone cancer pain.Methods Sixty-four pathogen-free healthy adult female unmated Sprague-Dawley rats,weighing 160-200 g,were divided into 2 groups (n=32 each) using a random number table:sham operation group (group S) and bone cancer pain group (group BP).Bone cancer pain was induced by injecting breast cancer cells into the abdominal cavity.The mechanical paw withdrawal threshold (MWT) was measured at 1 day before inoculating breast cancer cells and 7,14 and 21 days after inoculation (T0-3).Eight rats were sacrificed after measurement of MWT,and their lumbar enlargement segments of the spinal cord were removed for determination of Piezo2 expression by Western blot and immunofluorescence.The coexpression of Piezo2 with the neuronal marker NeuN,microglial marker Iba-1 and astrocyte marker GFAP was detected at T2 using double immunofluorescent staining.Results Compared with group S,the MWT was significandy decreased at T1-3,and the Piezo2 expression in the lumbar enlargement segment of the spinal cord was up-regulated in group BP (P ＜ 0.05).Piezo2 was mainly expressed in the spinal lamina Ⅰ and Ⅱ and co-expressed with NeuN and rarely co-expressed with GFAP or Iba-1.Conclusion The development and maintenance of bone cancer pain are related to up-regulated expression of Piezo2 in the lumbar enlargement segment of the spinal cord in rats.