To investigate the malignant progression and molecular mechanism of KHSRP regulating esophageal squamous cell carcinoma(ESCC) through the JAK1/STAT3 signaling axis.

Objective To investigate how KHSRP regulates the malignant development process of cardia gastric cancer through JAK1/STAT3 signaling pathway,and to reveal the molecular mechanisms.Methods Quantitative real-time fluores-cence polymerase chain reaction(qRT-PCR)was used to detect KHSRP in cancer cell lines(MKN-28,OE-33,HGC-27,KYSE-50,CRL-5822,SNU-1)as well as human normal epithelial cell lines(GES-1).Cell counting kit-8(CCK-8)and Transwell assay were used to detect the biological characteristics of cell proliferation,migration and invasion,respectively.Experimental subjects were divided into four groups in cellular and animal experiments:Sh-KHSRP group(KHSRP knockdown group),Sh-NC group(KHSRP control group),KHSRP group(KHSRP overexpression group),Vector group(KHSRP control group).The expres-sion levels of JAK/STAT and KHSRP proteins in stably transfected cells were detected by Western blotting.The mRNA and protein expression levels of KHSRP in different experimental groups were determined by real-time fluorescence quantitative PCR.Nude mouse experiments were performed to analyze the role of KHSRP in living animals.Results The qRT-PCR showed that the expression of KHSRP was significantly elevated in cancer cell lines(MKN-28,OE-33,HGC-27,KYSE-50,CRL-5822,SNU-1)and tumor tissues compared with human normal epithelial cells(GES-1)and tissues.The results of cell function experi-ments showed that knockdown of OE-33 and HGC-27 cell lines(sh-KHSRP group)significantly inhibited cell proliferation,mi-gration,and invasive ability,whereas the control group(sh-NC group)did not exhibit this inhibitory effect.These features were significantly enhanced in KHSRP overexpressing cells.In nude mice experiments,knockdown of KHSRP in nude mice led to re-duction in tumor volume and weight,lower cell proliferation rate,and lower number of lung nodal metastases compared with the control group(sh-NC group).These changes were reversed while KHSRP was overexpressed.Signaling pathway experiments showed that the expression of JAK1 and STAT3 was significantly downregulated in the sh-KHSRP group compared to the sh-NC group,with opposite results in the overexpression group.The results of cell rescue assay indicated that KHSRP promoted the proliferation,migration and invasion ability of cardia gastric cancer cells by regulating the JAK1/STAT3 signaling path-way.Conclusion KHSRP promotes the malignant process of cardia gastric cancer metastasis by regulating the JAK1/STAT3 signaling axis.

Objective To investigate how KHSRP regulates the malignant development process of cardia gastric cancer through JAK1/STAT3 signaling pathway,and to reveal the molecular mechanisms.Methods Quantitative real-time fluores-cence polymerase chain reaction(qRT-PCR)was used to detect KHSRP in cancer cell lines(MKN-28,OE-33,HGC-27,KYSE-50,CRL-5822,SNU-1)as well as human normal epithelial cell lines(GES-1).Cell counting kit-8(CCK-8)and Transwell assay were used to detect the biological characteristics of cell proliferation,migration and invasion,respectively.Experimental subjects were divided into four groups in cellular and animal experiments:Sh-KHSRP group(KHSRP knockdown group),Sh-NC group(KHSRP control group),KHSRP group(KHSRP overexpression group),Vector group(KHSRP control group).The expres-sion levels of JAK/STAT and KHSRP proteins in stably transfected cells were detected by Western blotting.The mRNA and protein expression levels of KHSRP in different experimental groups were determined by real-time fluorescence quantitative PCR.Nude mouse experiments were performed to analyze the role of KHSRP in living animals.Results The qRT-PCR showed that the expression of KHSRP was significantly elevated in cancer cell lines(MKN-28,OE-33,HGC-27,KYSE-50,CRL-5822,SNU-1)and tumor tissues compared with human normal epithelial cells(GES-1)and tissues.The results of cell function experi-ments showed that knockdown of OE-33 and HGC-27 cell lines(sh-KHSRP group)significantly inhibited cell proliferation,mi-gration,and invasive ability,whereas the control group(sh-NC group)did not exhibit this inhibitory effect.These features were significantly enhanced in KHSRP overexpressing cells.In nude mice experiments,knockdown of KHSRP in nude mice led to re-duction in tumor volume and weight,lower cell proliferation rate,and lower number of lung nodal metastases compared with the control group(sh-NC group).These changes were reversed while KHSRP was overexpressed.Signaling pathway experiments showed that the expression of JAK1 and STAT3 was significantly downregulated in the sh-KHSRP group compared to the sh-NC group,with opposite results in the overexpression group.The results of cell rescue assay indicated that KHSRP promoted the proliferation,migration and invasion ability of cardia gastric cancer cells by regulating the JAK1/STAT3 signaling path-way.Conclusion KHSRP promotes the malignant process of cardia gastric cancer metastasis by regulating the JAK1/STAT3 signaling axis.

Objective To investigate the regulatory effect of KHSRP on progression of gastric adenocarcinoma and the role of the JAK1/STAT3 signaling axis in mediating its effect.Methods KHSRP mRNA expression level was detected using qRT-PCR in 120 pairs of gastric adenocarcinoma and adjacent tissues,4 gastric adenocarcinoma cell lines(MKN-28,HGC-27,CRL-5822,and SNU-1)and normal human gastric mucosal GES-1 cells.In HGC-27 cells with KHSRP knockdown and SNU-1 cells with KHSRP overexpression,cell proliferation,migration,invasion and expression levels of JAK/STAT were evaluated using CCK-8 assay,Transwell migration and invasion assays,and Western blotting.In BALB/c-nude mice,HGC-27 cells with KHSRP knockdown and SNU-1 cells overexpressing KHSRP were injected either subcutaneous or via the tail vein to observe subcutaneous xenograft growth and lung metastasis of the tumor cells.Results Gastric adenocarcinoma tissues and cell lines all showed significantly increased KHSRP expression as compared with the adjacent tissues and GES-1 cells.In HGC-27 cells,KHSRP knockdown significantly inhibited cell proliferation,migration and invasion,while KHSRP overexpression enhanced the malignant behaviors of SNU-1 cells.In nude mice,inoculation of HGC-27 cells with KHSRP knockdown resulted in smaller tumor volume and weight,slower cell proliferation rate and fewer lung metastatic foci,and KHSRP-overexpressing SNU-1 cells produced the opposite results.KHSRP knockdown in HGC-27 cells significantly down-regulated the expression levels of JAK1 and STAT3,which were obviously increased in KHSRP-overexpressing SNU-1 cells.Conclusion High expressions of KHSRP promote progression and metastasis of gastric adenocarcinoma possibly by regulating the JAK1/STAT3 signaling axis.

Objective To investigate the regulatory effect of KHSRP on progression of gastric adenocarcinoma and the role of the JAK1/STAT3 signaling axis in mediating its effect.Methods KHSRP mRNA expression level was detected using qRT-PCR in 120 pairs of gastric adenocarcinoma and adjacent tissues,4 gastric adenocarcinoma cell lines(MKN-28,HGC-27,CRL-5822,and SNU-1)and normal human gastric mucosal GES-1 cells.In HGC-27 cells with KHSRP knockdown and SNU-1 cells with KHSRP overexpression,cell proliferation,migration,invasion and expression levels of JAK/STAT were evaluated using CCK-8 assay,Transwell migration and invasion assays,and Western blotting.In BALB/c-nude mice,HGC-27 cells with KHSRP knockdown and SNU-1 cells overexpressing KHSRP were injected either subcutaneous or via the tail vein to observe subcutaneous xenograft growth and lung metastasis of the tumor cells.Results Gastric adenocarcinoma tissues and cell lines all showed significantly increased KHSRP expression as compared with the adjacent tissues and GES-1 cells.In HGC-27 cells,KHSRP knockdown significantly inhibited cell proliferation,migration and invasion,while KHSRP overexpression enhanced the malignant behaviors of SNU-1 cells.In nude mice,inoculation of HGC-27 cells with KHSRP knockdown resulted in smaller tumor volume and weight,slower cell proliferation rate and fewer lung metastatic foci,and KHSRP-overexpressing SNU-1 cells produced the opposite results.KHSRP knockdown in HGC-27 cells significantly down-regulated the expression levels of JAK1 and STAT3,which were obviously increased in KHSRP-overexpressing SNU-1 cells.Conclusion High expressions of KHSRP promote progression and metastasis of gastric adenocarcinoma possibly by regulating the JAK1/STAT3 signaling axis.

Objective    To investigate the preoperative localization of pulmonary glabrous nodules. Methods    A total of 192 patients admitted to General Hospital of  Northern Theater Command from April 2012 to September 2019 were selected for the study. There were 95 males and 97 females at an age of 56.47±11.79 years. All patients completed preoperative examination, and were divided into a positioning group (n=97) and a non-positioning group (n=95) according to whether the preoperative positioning was performed. And the surgical indicators between the two groups were compared. According to the substance of ground-glass opacity, they were divided into a pure ground-glass nodules group (n=23) and a mixed ground-glass nodules group (n=74) in the positioning group and a pure ground-glass nodules group (n=14) and a mixed ground-glass nodules group (n=81) in the non-positioning group . According to the size and distance of the nodules from the pleura and whether the nodules could be detected, the corresponding linear function was obtained. Results    The operative time of methylene blue localization group was shorter than that of the no localization group. In the scatter plot, the corresponding diameter and depth of the nodules and the corresponding coordinate points which can be explored were described. And linear regression was performed on all the coordinate points to obtain the linear function: depth=0.648×diameter–1.446 (mm). It can be used as an indication for the preoperative localization of pure ground-glass nodules in Da Vinci robotic surgery. Linear function: depth=0.559 5×diameter+0.56 (mm). It can be used as an indication of preoperative localization of mixed ground-glass nodules in Da Vinci robotic surgery. Conclusion    This equation can be used as a preoperative indication for clinical peripheral pulmonary ground-glass nodules.