Objective To investigate the effect and mechanism of oxycodone on the treatment of cancerous neuropathic pain in advanced colon cancer.Methods 80 cases of advanced colon cancer in department of anorectal of Shaoxing Second Hospital of Zhejiang Province from March 2015 to March 2016 were selected and randomly divided into two groups with 40 cases in each group.The control group were treated with routine clinical treatment, and the experiment group were treated with oxycodone treatment on the basis of the control group.The levels of pain score, quality of life score, serum β-EP, calcitonin gene related peptide (CGRP) and prostaglandin E2(PGE2), clinical efficacy and adverse reaction incidence rate changes were compared between two groups before and after treatment.Results Compared with before treatment, levels of the pain score, serum β-EP, CGRP and PGE2 decreased in two groups after treatment, after treatment, the experiment group pain score (2.38 ±0.34), quality of life score (28.39 ± 3.97), serumβ-EP (228.71 ±34.92), CGRP (22.46 ±3.15), PGE2 level (2.45 ±0.35) and the incidence of adverse reactions was 17.50%, were lower than that of the control group the pain score (3.51 ±0.51), the quality of life score (33.53 ±4.76), serum β-EP (246.67 ±34.83), CGRP (30.36 ±4.25), PGE2(3.36 ±0.47) and the incidence of adverse reactions was 40.00%, the difference was statistically significant (P<0.05), the total effective rate of the experiment group was 87.50%, higher than that of the control group, the total effective rate was 60.00%, the difference was statistically significant (P<0.05).Conclusion Oxycodone can effectively reduce pain in patients with advanced colon cancer neuropathic pain score, improve the quality of life, and has high clinical efficacy and safety.

Objective To elucidate the relative level of miR-23a RNA in rectal cancer tissues and cell line as well as the effects of miR-23a on the cell proliferation and apoptosis of rectal cancer cells in vitro.Methods Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was applied in assessment of the transcription of miR-23a in rectal cancer tissues and in vitro cells.The RNA fragment of miR-23a inhibitor and inhibitor NC were synthesized and transfected into SW480 cells.Cell proliferation was evaluated with Cell Counting Kit-8 (CCK-8) assay.The apoptotic rate was analyzed by flow cytometry.The expression of ESRP1 was detected by western blot.Wild-type pGL3-ESRP1-3'UTR (wt-pGL3-ESRP1-3'UTR) or mutant pGL3-ESRP1-3'UTR (mut-pGL3-ES-RP1-3'UTR) plasmids and miR-23a inhibitor RNA fragments or inhibitor NC RNA fragments were co-transfected into HEK293 and SW480 cells,then the Promega dual luciferase reporter gene assay kit was used to examine the dual luciferase activity in SW480 cells.Resuits The relative RNA level of miR-23a was significantly promoted in both rectal cancer tissue samples and SW480 cells.After SW480cells were transfected with miR-23a inhibitor,human rectal cancer cell line SW480 with down-regulation of miR-23a showed significant inhibition of cell proliferation compared with negative control (P =0.000).Furthermore,our data demonstrated clearly that the inhibition of miR-23a promoted apoptosis in SW480 cells (P =0.000).Luciferase assay showed that ESRP1 was a direct target gene of miR -23a.Conclusion The expression of miR-23a is clearly associated with the growth and apoptosis of human rectal cells by targeting ESRP1,whilst miR-23a may be used as a potential therapeutic target for the treatment of rectal cancer in the future.

AIM:To investigate the expression of miR-23a and epithelial splicing regulatory protein 1(ESRP1) in rectal cancer tissues and cell lines as well as their effects on rectal cancer cell viability and apoptosis.METHODS:The relative levels of miR-23a in the rectal cancer tissues and cultured cells were assessed by RT-qPCR.The positive expression of ESRP1 in the rectal cancer tissues and non-cancer tissues was detected by immunohistochemical staining.The sequences of miR-23a inhibitor and inhibitor negative control (NC) were synthesized, and transfected into the SW480 cells.The cell viability was measured by CCK-8 assay.The apoptotic rate was analyzed by flow cytometry.The cell invasion was evaluated by Matrigel counting assay.The expression of ESRP1 was determined by Western blot.The wild-type pGL3-ESRP1-3'UTR (wt-pGL3-ESRP1-3'UTR) or mutant pGL3-ESRP1-3'UTR (mut-pGL3-ESRP1-3'UTR) plasmid and miR-23a inhibitor or inhibitor NC were co-transfected into the HEK293 and SW480 cells.The dual luciferase activity was detected according to Promega dual luciferase reporter gene assay kit instructions.The cell viability and apoptosis were evaluated by CCK-8 assay and flow cytometry analysis, respectively, after the SW480 cells were transfected with ESRP1 mimic or mimic NC.The expression of ESRP1, caspase-3, Smac and X-linked inhibitor of apoptosis protein (XIAP) in the SW480 cells was detected by Western blot.RESULTS:The expression of miR-23a was significantly up-re-gulated in the rectal cancer tissues and cell lines, while the positive expression of ESRP1 was significantly decreased in the rectal cancer specimens.The miR-23a expression was also closely related to lymphnode metastasis and TNM stages of rectal cancer patients.ESRP1 was inversely correlated with miR-23a in the rectal cancer tissues.After transfection with miR-23a inhibitor in human rectal cancer SW480 cells, the down-regulation of miR-23a induced significant inhibition of cell viability as compared with the cells transfected with inhibitor NC (P<0.01).Furthermore, the apoptotic rate induced by the miR-23a inhibitor transfection was markedly higher than that of control (P<0.01).Luciferase assay showed that ESRP1 was a direct target gene of miR-23a.The cell viability and apoptosis were inhibited and promoted, respectively, after transfection with ESRP1 mimic in the SW480 cells.Promoted expression of ESRP1 significantly up-regulated the levels of caspase-3 and Smac as well as down-regulated the expression of XIAP in the SW480 cells.CONCLUSION:The expression of miR-23a is significantly associated with the growth and apoptosis of human rectal cancer cells by targeting ESRP1.miR-23a may be a potential therapeutic target for the treatment of rectal cancer in the future.

A total of 225 patients with colorectal cancer (CRC) admitted to the General Hospital of Shaoxing Second Hospital Medical community from May 5, 2020 to May 28, 2022 were enrolled (CRC group), and 101 healthy subjects underwent colorectal examination were selected as the control group. The tissue biopsy samples of all subjects were obtained by colonoscopy, and subjected to Sanger sequencing to determine the polymorphism sites of the syndecan-2 (SDC2) gene. The association between SDC single nucleotide polymorphism (SNP) and colorectal cancer in CRC patients was analyzed with logistic regression. The logistic regression analysis showed that the gene polymorphism of SDC2 rs2515127 was associated with colorectal cancer ( OR=1.643, 95% CI: 1.025-2.337, P=0.012). The frequency of GG, AG and AA the in genotypes of SDC2 rs2515127 was 60.7% (102/168), 30.4% (51/168) and 8.9% (15/168), respectively. The results showed that the gene polymorphism of SDC2 rs2515127 was associated with colorectal cancer, and the frequencies of GG and AG genotypes were higher in the genotypes of SDC2 rs2515127.