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1.
Asian J Androl ; 2023 Nov 07.
Article in English | MEDLINE | ID: mdl-37934170

ABSTRACT

ABSTRACT: To investigate the molecular etiology of low sperm quality in patients with intractable spermatocystitis, spermatozoa samples from patients with persistent hematospermia undergoing transurethral seminal vesiculoscopy and healthy volunteers were utilized. Spermatozoa samples were collected from the seminal vesicles through transurethral seminal vesiculoscopy or by masturbation ejaculation. Sperm quality was analyzed by a WLJY-9000 color semen analysis system. Measurement of tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6) in the seminal plasma was performed using enzyme-linked immunosorbent assay (ELISA). Measurement of H2O2 in the seminal plasma was performed with a hydrogen peroxide kit. The protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and phosphorylated-Nrf2 (p-Nrf2) were measured by western blot analysis and immunofluorescence assays. Low sperm quality parameters and increased levels of inflammatory cytokines (TNFα, IL-6, and H2O2) in the seminal plasma were detected among the semen samples from the patients with persistent hematospermia. Nrf2 and p-Nrf2 were strongly expressed in the nucleus and periphery of human sperm cells, according to the results of the immunofluorescence assays. The protein levels of Nrf2 and p-Nrf2 were significantly lower in the spermatozoa samples from patients with persistent hematospermia than in those from healthy volunteers with normal sperm motility. The results suggested that Nrf2 signaling might play a role in the low sperm quality of patients with intractable spermatocystitis.

2.
J Cancer ; 11(17): 5042-5055, 2020.
Article in English | MEDLINE | ID: mdl-32742452

ABSTRACT

Ubiquinol-cytochrome c reductase core protein 2 (UQCRC2) is an important mitochondrial complex III subunit. This study investigated the role of UQCRC2 in gastric cancer (GC) and its upstream regulatory microRNAs (miRNAs). UQCRC2 expression levels were lower in GC tissues than non-carcinoma tissues. Furthermore, UQCRC2 levels were negatively correlated with lymph node metastasis, relapse, and tumor grade. Bioinformatics analysis predicted UQCRC2 as the target gene for miR-370, and this was verified in luciferase reporter assays. MiR-370 levels were inversely correlated with UQCRC2 levels in GC. UQCRC2 overexpression suppressed GC cell migration and invasion in vitro and in vivo, whereas up-regulating miR-370 reversed these effects. Western blotting analysis showed that miR-370 targeted UQCRC2 and positively regulated the epithelial-mesenchymal transition (EMT) signaling pathway in GC cells. Therefore, the miR-370/UQCRC2 axis may regulate EMT signaling pathways to affect tumor proliferation and metastasis and is, thus, a potential target for GC treatment.

3.
J Cell Mol Med ; 24(18): 10842-10854, 2020 09.
Article in English | MEDLINE | ID: mdl-32757436

ABSTRACT

The aim of the present study was to explore the underlying mechanisms involved in gastric cancer (GC) formation using data-independent acquisition (DIA) quantitative proteomics analysis. We identified the differences in protein expression and related functions involved in biological metabolic processes in GC. Totally, 745 differentially expressed proteins (DEPs) were found in GC tissues vs. gastric normal tissues. Despite enormous complexity in the details of the underlying regulatory network, we find that clusters of proteins from the DEPs were mainly involved in 38 pathways. All of the identified DEPs involved in oxidative phosphorylation were down-regulated. Moreover, GC possesses significantly altered biological metabolic processes, such as NADH dehydrogenase complex assembly and tricarboxylic acid cycle, which is mostly consistent with that in KEGG analysis. Furthermore the higher expression of UQCRQ, NDUFB7 and UQCRC2 were positively correlated with a better prognosis, implicating these proteins may as novel candidate diagnostic and prognostic biomarkers.


Subject(s)
Adenocarcinoma/genetics , Gene Expression Regulation, Neoplastic , Neoplasm Proteins/genetics , Oxidative Phosphorylation , Proteomics/methods , Stomach Neoplasms/genetics , Adenocarcinoma/diagnosis , Adenocarcinoma/metabolism , Adenocarcinoma/mortality , Adult , Aged , Biomarkers, Tumor , Down-Regulation , Female , Gastric Mucosa/metabolism , Gene Regulatory Networks , Humans , Kaplan-Meier Estimate , Male , Metabolic Networks and Pathways/genetics , Middle Aged , Neoplasm Proteins/biosynthesis , Precancerous Conditions/genetics , Precancerous Conditions/metabolism , Precancerous Conditions/mortality , Prognosis , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , RNA, Neoplasm/biosynthesis , RNA, Neoplasm/genetics , Stomach Neoplasms/diagnosis , Stomach Neoplasms/metabolism , Stomach Neoplasms/mortality , Tandem Mass Spectrometry , Tumor Microenvironment
4.
J Huazhong Univ Sci Technolog Med Sci ; 37(6): 880-885, 2017 Dec.
Article in English | MEDLINE | ID: mdl-29270747

ABSTRACT

The Grainyhead-like 3 (GRHL3) is involved in epidermal barrier formation, neural tube closure and wound repair. Previous studies have suggested that GRHL3 has been linked to many different types of cancers. However, to date, its effects on human colorectal cancer (CRC) has not been clarified yet. Our microarray analysis has indicated predominant GRHL3 expression in CRC. The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues, as well as using distinct CRC cell lines (HT29 and DLD1). We observed increased GRHL3 expression at both mRNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Moreover, silencing GRHL3 with siRNA could suppress CRC cell proliferation, viability and migration in vitro. We also found that knockdown of GRHL3 could promote cell cycle arrest at G0/G1 phase in HT29 cells and DLD1 cells, and induce cell apoptosis in HT29 cells. Together, our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G0/G1 phase and apoptosis.


Subject(s)
Cell Cycle Checkpoints/genetics , Colorectal Neoplasms/genetics , DNA-Binding Proteins/genetics , Gene Expression Regulation, Neoplastic , Transcription Factors/genetics , Apoptosis/genetics , Cell Line, Tumor , Cell Movement , Cell Proliferation , Colorectal Neoplasms/metabolism , Colorectal Neoplasms/pathology , DNA-Binding Proteins/antagonists & inhibitors , DNA-Binding Proteins/metabolism , Gene Expression Profiling , HCT116 Cells , HT29 Cells , Humans , Microarray Analysis , RNA, Small Interfering/genetics , RNA, Small Interfering/metabolism , Transcription Factors/antagonists & inhibitors , Transcription Factors/metabolism
5.
J Huazhong Univ Sci Technolog Med Sci ; 37(3): 343-347, 2017 Jun.
Article in English | MEDLINE | ID: mdl-28585149

ABSTRACT

The sialyl Lewis X (SLex) antigen encoded by the FUT7 gene is the ligand of endotheliam-selectin (E-selectin). The combination of SLex antigen and E-selectin represents an important way for malignant tumor metastasis. In the present study, the effect of the SLex-binding DNA aptamer on the adhesion and metastasis of hepatocellular carcinoma HepG2 cells in vitro was investigated. Reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence staining were conducted to detect the expression of FUT7 at both transcriptional and translational levels. The SLex expression in HepG2 cells treated with different concentrations of SLex-binding DNA aptamer was detected by flow cytometry. Besides, the adhesion, migration, and invasion of HepG2 cells were measured by cell adhesion assay, and the Transwell migration and invasion assay. The results showed that the FUT7 expression was up-regulated at both mRNA and protein levels in HepG2 cells. SLex-binding DNA aptamer could significantly decrease the expression of SLex in HepG2 cells. The cell adhesion assay revealed that the SLex-binding DNA aptamer could effectively inhibit the interactions between E-selectin and SLex in the HepG2 cells. Additionally, SLex-binding DNA aptamers at 20 nmol/L were found to have the similar effect to the monoclonal antibody CSLEX-1. The Transwell migration and invasion assay revealed that the number of penetrating cells on the down-side of Transwell membrane was significantly less in cells treated with 5, 10, 20 nmol/L SLex-binding DNA aptamer than those in the negative control group (P<0.01). Our study demonstrated that the SLex-binding DNA aptamer could significantly inhibit the in vitro adhesion, migration, and invasion of HepG2 cells, suggesting that the SLex-binding DNA aptamer may be used as a potential molecular targeted drug against metastatic hepatocellular carcinoma.


Subject(s)
Aptamers, Nucleotide/genetics , E-Selectin/genetics , Fucosyltransferases/genetics , Gene Expression Regulation, Neoplastic , Lewis X Antigen/genetics , Aptamers, Nucleotide/metabolism , Cell Adhesion , Cell Movement , Diffusion Chambers, Culture , E-Selectin/metabolism , Fucosyltransferases/antagonists & inhibitors , Fucosyltransferases/metabolism , Hep G2 Cells , Humans , Lewis X Antigen/antagonists & inhibitors , Lewis X Antigen/metabolism , Protein Biosynthesis , Sialyl Lewis X Antigen , Transcription, Genetic
6.
J Huazhong Univ Sci Technolog Med Sci ; 37(1): 30-36, 2017 Feb.
Article in English | MEDLINE | ID: mdl-28224429

ABSTRACT

Current studies have demonstrated that SLC38A1 proteins play a causal role in neoplastic cell transformation. The twofold aim of this study was to provide insight into whether a variance in the expression of SLC38A1 exists between human colorectal cancer and healthy human tissues and to determine how silencing or overexpressing the SLC38A1 gene could affect the proliferation, viability and migration of colorectal cancer cells. Immunohistochemical staining was used to analyze the expression of SLC38A1 in colorectal cancer tissues and adjacent normal mucosa in 77 patients who underwent surgical resection. The expression of SLC38A1 in colorectal cancer tissues and cell lines was detected using RT-PCR and Western blotting. Two colorectal cancer cell lines SW480 and HCT116 were used to examine whether silencing SLC38A1 with siRNA and overexpressing SLC38A1 with shRNA could affect cell viability and migration. As a result, the SLC38A1 protein was very low or undetectable in the normal colon mucosa. In contrast, strong staining of SLC38A1 protein was found in the cytoplasm in 79.2% colorectal cancer samples. More pronounced SLC38A1 expression in colorectal cancer tissues was significantly associated with tumor node metastasis (TNM) stage. Inhibition of SLC38A1 reduced tumour growth and suppressed proliferation and migration of SW480 cells. In contrast, overexpression of SLC38A1 had the opposite effects on HCT116 cells. SLC38A1 is overexpressed in colorectal cancer, which suggests that it is associated with tumour progression. These results encourage the exploration of SLC38A1 as a target for intervention in colorectal cancer.


Subject(s)
Amino Acid Transport System A/genetics , Amino Acid Transport System A/metabolism , Colorectal Neoplasms/pathology , Cytoplasm/metabolism , Cell Line, Tumor , Cell Movement , Cell Proliferation , Colorectal Neoplasms/genetics , Colorectal Neoplasms/metabolism , Cytoplasm/genetics , Female , Gene Expression Regulation, Neoplastic , HCT116 Cells , Humans , Male , Neoplasm Staging , Up-Regulation
7.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-333475

ABSTRACT

The sialyl Lewis X (SLex) antigen encoded by the FUT7 gene is the ligand of endotheliam-selectin (E-selectin).The combination of SLex antigen and E-selectin represents an important way for malignant tumor metastasis.In the present study,the effect of the SLeX-binding DNA aptamer on the adhesion and metastasis of hepatocellular carcinoma HepG2 cells in vitro was investigated.Reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence staining were conducted to detect the expression of FUT7 at both transcriptional and translational levels.The SLex expression in HepG2 cells treated with different concentrations of SLeX-binding DNA aptamer was detected by flow cytometry.Besides,the adhesion,migration,and invasion of HepG2 cells were measured by cell adhesion assay,and the Transwell migration and invasion assay.The results showed that the FUT7 expression was up-regulated at both mRNA and protein levels in HepG2 cells.SLeX-binding DNA aptamer could significantly decrease the expression of SLex in HepG2 cells.The cell adhesion assay revealed that the SLeX-binding DNA aptamer could effectively inhibit the interactions between E-selectin and SLex in the HepG2 cells.Additionally,SLeX-binding DNA aptamers at 20 nmol/L were found to have the similar effect to the monoclonal antibody CSLEX-1.The Transwell migration and invasion assay revealed that the number of penetrating cells on the down-side of Transwell membrane was significantly less in cells treated with 5,10,20 nmol/L SLeX-binding DNA aptamer than those in the negative control group (P<0.01).Our study demonstrated that the SLeX-binding DNA aptamer could significantly inhibit the in vitro adhesion,migration,and invasion of HepG2 cells,suggesting that the SLeX-binding DNA aptamer may be used as a potential molecular targeted drug against metastatic hepatocellular carcinoma.

8.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-333410

ABSTRACT

The Grainyhead-like 3 (GRHL3) is involved in epidermal barrier formation,neural tube closure and wound repair.Previous studies have suggested that GRHL3 has been linked to many different types of cancers.However,to date,its effects on human colorectal cancer (CRC) has not been clarified yet.Our microarray analysis has indicated predominant GRHL3 expression in CRC.The purpose of this study was to investigate the expression and significance of GRHL3 in CRC tumorigenesis using CRC tissues and paired paracancerous tissues,as well as using distinct CRC cell lines (HT29 and DLD1).We observed increased GRHL3 expression at both mRNA and protein levels in CRC tissues and CRC cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting.Moreover,silencing GRHL3 with siRNA could suppress CRC cell proliferation,viability and migration in vitro.We also found that knockdown of GRHL3 could promote cell cycle arrest at G0/G1 phase in HT29 cells and DLD1 cells,and induce cell apoptosis in HT29 cells.Together,our study revealed the down-regulation of GRHL3 in vitro could inhibit CRC cell activity and trigger cell cycle arrest at G0/G1 phase and apoptosis.

9.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-238397

ABSTRACT

Current studies have demonstrated that SLC38A1 proteins play a causal role in neoplastic cell transformation.The twofold aim of this study was to provide insight into whether a variance in the expression of SLC38A1 exists between human colorectal cancer and healthy human tissues and to determine how silencing or overexpressing the SLC38A1 gene could affect the proliferation,viability and migration of colorectal cancer cells.Immunohistochemical staining was used to analyze the expression of SLC38A1 in colorectal cancer tissues and adjacent normal mucosa in 77 patients who underwent surgical resection.The expression of SLC38A1 in colorectal cancer tissues and cell lines was detected using RT-PCR and Western blotting.Two colorectal cancer cell lines SW480 and HCT116 were used to examine whether silencing SLC38A1 with siRNA and overexpressing SLC38A1 with shRNA could affect cell viability and migration.As a result,the SLC38A1 protein was very low or undetectable in the normal colon mucosa.In contrast,strong staining of SLC38A1 protein was found in the cytoplasm in 79.2% colorectal cancer samples.More pronounced SLC38A1 expression in colorectal cancer tissues was significantly associated with tumor node metastasis (TNM) stage.Inhibition of SLC38A1 reduced tumour growth and suppressed proliferation and migration of SW480 cells.In contrast,overexpression of SLC38A1 had the opposite effects on HCT116 cells.S LC38A1 is overexpressed in colorectal cancer,which suggests that it is associated with tumour progression.These results encourage the exploration of SLC38A1 as a target for intervention in colorectal cancer.

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