Objective:To investigate the effects of enolase 1(ENO1)on the proliferation,migration,and invasion of gastric cancer cells and its underlying molecular mechanisms.Methods:The expression levels of ENO1 in human gastric cancer cell lines(HGC27,MKN-45,N-87,MGC803,BGC-823)and human gastric mucosal epithelial cells(GES-1)were detected using WB assay.Gene editing tools such as CRISPR and overexpression system were used to construct ENO1 knockdown and knockdown-rescue cell lines.Both MKN-45 and BGC-823 cells were grouped into control(Ctrl)group,ENO1 knockdown(ENO1 KD)group,and ENO1 knockdown-rescue(ENO1 KD-OE)group.The effects of ENO1 knockdown or ENO1 knockdown-rescue on the proliferation,migration,invasion,and apoptosis of gastric cancer cells were evaluated using colony formation assay,EdU staining,scratch wound healing assay,Transwell chamber assay and flow cytometry.Additionally,a xenograft model was established in nude mice,and the effects of ENO1 on tumor growth were monitored using small animal in vivo imaging and tumor tissue block measurement.ENO1 was silenced in MKN-45 cells employing RNA interference technology,and the downstream target genes of ENO1 were identified using RNA co-immunoprecipitation sequencing(RIP-seq)and bioinformatics analysis.The molecular mechanisms by which ENO1 regulates the proliferation,migration and invasion of gastric cancer cells was also analyzed.Results:ENO1 was significantly upregulated in gastric cancer cell lines(P<0.01 or P<0.001).ENO1 knockdown significantly inhibited proliferation,migration,and invasion while promoting apoptosis in MKN-45 and BGC-823 cells(P<0.001,P<0.000 1).Rescue experiments showed that restoring ENO1 expression significantly enhanced cell proliferation,migration,invasion,and inhibited apoptosis(P<0.05,P<0.01,P<0.001,P<0.000 1).In vivo experiments demonstrated that ENO1 knockdown significantly inhibited tumor growth in nude mice(P<0.000 1).The differentially expressed genes interacting with ENO1 protein were primarily enriched in pathways related to RNA splicing.Additionally,ENO1 protein was found to interact with the PKM gene,and their expressions showed a positive correlation in gastric cancer tissues(r=0.886).Conclusion:ENO1 is highly expressed in gastric cancer cells.ENO1 interacts with precursor mRNA of PKM to influence its RNA splicing process,thereby regulating PKM2 expression and promoting gastric cancer progression.

Objective To quantitatively evaluate the association between Ile105Val polymorphism of glutathione S-transferase pi (GSTP1) and sensitivity to platinum-based chemotherapy in advanced gastric cancer.Methods The relevant published literatures about Ile105Val polymorphism of GSTP1 and sensitivity to platinum-based chemotherapy in gastric cancer were retrieved from China National Knowledge Internet (CNKI),VIP,Chinese Biomedical Literature Data (CBM),Wan-Fang databases,PubMed,EMBASE and Cochrane Library.Clinical response (complete response and partial response) was employed to estimate chemosensitivity.Meta-analysis was conducted by the RevMan 5.2 software,odds ratio (OR) with 95％ confidence interval (CI) were calculated.Publication bias was identified using Stata 12.0 software.Results A total of 724 cases from 6 case-control trials were included.The results of Meta-analysis showed the different statistical significance was found between GSTP1 Ilel05Val polymorphism and clinical response in the follow genotypes [GG+GA vs AA:OR =2.38,95％CI (1.29 ～4.38); GG vs GA + AA:OR =3.66,95％CI (1.18 ～11.39) ; GG vs AA:OR =4.42,95％ CI (1.28 ～ 15.26)] and Asian population subgroups [GG + GAvs AA:OR =2.93,95％ CI (1.33 ～ 6.48)].Conclusion Polymorphism of GSTP1 Ile105Val(A/G) may be associated with platinum-based chemosensitivity in advanced gastric cancer.

OBJECTIVE:To discuss ward drug control to ensure safe.METHODS:We analyzed retrospectively the application of 5S theory in ward drug control.RESULTS & CONCLUSION:By this drug control mode,drugs were classified according to varieties,usage,frequency of use etc,drug control quality and work efficiency were enhanced,patients' needs could be satisfies and staff' s professional quality was enhanced.

BACKGROUNDTo study the clinical effects of ¹⁵³Sm-EDTMP plus chemotherapy in the treatment of bone metastasis of lung cancer.

METHODSOne hundred and ten lung cancer patients with one metastasis [male 82 and female 28, aged from 32 to 76 yrs; squamous cell carcinoma 28, adenocarcinoma 27, small cell lung cancer (SCLC) 7, mix type 41, alveolar carcinoma 7] who did not undergo an operation were entered into this study. The patients were divided into 3 groups: ¹⁵³Sm-EDTMP therapy only (37 cases), ¹⁵³Sm-EDTMP plus chemotherapy after 3 days (42 cases), 30 days after chemotherapy plus ¹⁵³Sm-EDTMP (31 cases). The dosages of ¹⁵³Sm-EDTMP ranged from 1 111 to 2 660 MBq. The patients with SCLC were adapted CCNU, MTX and CTX; those with non-small cell lung cancer (NSCLC) were adapted MMC, VCR and DDP. Statistic analysis of the data was performed by Chi-square test.

RESULTSTotal pain relief rate for ¹⁵³Sm-EDTMP only was 89.2% , for ¹⁵³Sm-EDTMP plus chemotherapy was 92.8%, and for chemotherapy plus 153 Sm EDTMP was 90.3% . The foci disappeared in 9 cases with ¹⁵³Sm-EDTMP only, in 12 cases with ¹⁵³Sm-EDTMP plus chemotherapy, and in 9 cases with chemotherapy plus ¹⁵³Sm-EDTMP. The 1 year survival rate was 29.7%(11/37) by 153 Sm only, 40.5%(17/42) by 153 Sm plus chemotherapy, 38.7%(12/31) by chemotherapy plus ¹⁵³Sm-EDTMP.

CONCLUSIONS¹⁵³Sm-EDTMP plus chemotherapy is effective in the treatment of bone metastasis of lung cancer.