Aim To investigate the effect of benzyl iso-thiocyanate (BITC) on the proliferation of mouse U14 cervical cancer cells and to explore the mechanism of cytotoxicity based on transcriptomic data analysis. Methods The effect of BITC on U14 cell activity was detected by MTT, nuclear morphological changes were observed by Hochest 33258 and fluorescent inverted microscope, cell cycle and apoptosis were determined by flow cytometry, and the transcriptome database of U14 cells before and after BITC (20 μmol · L

Objective To evaluate the relationship between diabetic nephropathy(DN)and diabetic retinopathy(DR)in patients with type 2 diabetes mellitus(T2DM)based on imaging and clinical testing data.Methods Totally 600 T2DM patients who visited the First People's Hospital of Ziyang from March 2021 to December 2022 were included.The fundus photography and fundus fluorescein angiography were performed on all these patients and their age,gender,T2DM duration,cardiovascular diseases,cerebrovascular disease,hypertension,smoking history,drinking history,body mass in-dex,systolic blood pressure,diastolic blood pressure and other clinical data were collected.The levels of fasting blood glu-cose(FPG),triglyceride(TG),total cholesterol(TC),high-density lipoprotein cholesterol(HDL-C),low-density lipo-protein cholesterol(LDL-C),glycosylated hemoglobin(HbA1c),24 h urinary albumin(UAlb),urinary albumin to creati-nine ratio(ACR),serum creatinine(Scr)and blood urea nitrogen(BUN)were measured.Logistic regression was used to analyze the risk factors associated with DR.DR staging was performed according to fundus images,and the convolutional neural network(CNN)algorithm was used as an image analysis method to explore the correlation between DR and DN based on emission computed tomography(ECT)and clinical testing data.Results The average lesion area rates of DR and DN detected by the CNN in the non-DR,mild-non-proliferative DR(NPDR),moderate-NPDR,severe-NPDR and pro-liferative DR(PDR)groups were higher than those obtained by the traditional algorithm(TCM).As DR worsened,the Scr,BUN,24 h UAlb and ACR gradually increased.Besides,the incidence of DN in the non-DR,mild-NPDR,moderate-NPDR,severe-NPDR and PDR groups was 1.67％,8.83％,16.16％,22.16％and 30.83％,respectively.Logistic regression analysis showed that the duration of T2DM,smoking history,HbA1c,TC,TG,HDL-C,LDL-C,24 h UAlb,Scr,BUN,ACR and glomerular filtration rate(GFR)were independent risk factors for DR.Renal dynamic ECT analysis demonstrated that with the aggravation of DR,renal blood flow perfusion gradually decreased,resulting in diminished renal filtration.Conclusion The application of CCN in the early stage DR and DN image analysis of T2DM patients will improve the diag-nosis accuracy of DR and DN lesion area.The DN is worsening as the aggravation of DR.

Wnt signaling are critical pathway involved in organ development, tumorigenesis, and cancer progression. WNT7A, a member of the Wnt family, remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma (HNSCC). According to the Cancer Genome Atlas (TCGA), transcriptome sequencing data of HNSCC, the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues, which was validated using Real-time RT-PCR and immunohistochemistry. Unexpectedly, overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC. Instead, our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway, leading to enhanced cell proliferation, self-renewal, and resistance to apoptosis. Furthermore, in a patient-derived xenograft (PDX) tumor model, high expression of WNT7A and phosphorylated STAT3 was observed, which positively correlated with tumor progression. These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.
Animals ; Humans ; Squamous Cell Carcinoma of Head and Neck ; Carcinogenesis/genetics* ; Cell Transformation, Neoplastic ; Wnt Signaling Pathway ; Disease Models, Animal ; Head and Neck Neoplasms/genetics* ; Wnt Proteins ; Frizzled Receptors/genetics* ; Janus Kinase 1 ; STAT3 Transcription Factor

OBJECTIVE: To determine the role of Tripterygium wilfordii multiglycoside (TGW) in the treatment of psoriatic dermatitis from a cellular immunological perspective. METHODS: Mouse models of psoriatic dermatitis were established by imiquimod (IMQ). Twelve male BALB/c mice were assigned to IMQ or IMQ₊TGW groups according to a random number table. Histopathological changes in vivo were assessed by hematoxylin and eosin staining. Ratios of immune cells and cytokines in mice, as well as PAM212 cell proliferation in vitro were assessed by flow cytometry. Pro-inflammatory cytokine expression was determined using reverse transcription quantitative polymerase chain reaction. RESULTS: TGW significantly ameliorated the severity of IMQ-induced psoriasis-like mouse skin lesions and restrained the activation of CD45⁺ cells, neutrophils and T lymphocytes (all P<0.01). Moreover, TGW significantly attenuated keratinocytes (KCs) proliferation and downregulated the mRNA levels of inflammatory cytokines including interleukin (IL)-17A, IL-23, tumor necrosis factor α, and chemokine (C-X-C motif) ligand 1 (P<0.01 or P<0.05). Furthermore, it reduced the number of γ δ T17 cells in skin lesion of mice and draining lymph nodes (P<0.01). CONCLUSIONS TGW improved psoriasis-like inflammation by inhibiting KCs proliferation, as well as the associated immune cells and cytokine expression. It inhibited IL-17 secretion from γ δ T cells, which improved the immune-inflammatory microenvironment of psoriasis.
Male ; Animals ; Mice ; Tripterygium ; Psoriasis/drug therapy* ; Keratinocytes ; Skin Diseases/metabolism* ; Cytokines/metabolism* ; Imiquimod/metabolism* ; Dermatitis/pathology* ; Disease Models, Animal ; Mice, Inbred BALB C ; Skin/metabolism*

Wnt signaling are critical pathway involved in organ development,tumorigenesis,and cancer progression.WNT7A,a member of the Wnt family,remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma(HNSCC).According to the Cancer Genome Atlas(TCGA),transcriptome sequencing data of HNSCC,the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues,which was validated using Real-time RT-PCR and immunohistochemistry.Unexpectedly,overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC.Instead,our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway,leading to enhanced cell proliferation,self-renewal,and resistance to apoptosis.Furthermore,in a patient-derived xenograft(PDX)tumor model,high expression of WNT7A and phosphorylated STAT3 was observed,which positively correlated with tumor progression.These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.

Wnt signaling are critical pathway involved in organ development,tumorigenesis,and cancer progression.WNT7A,a member of the Wnt family,remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma(HNSCC).According to the Cancer Genome Atlas(TCGA),transcriptome sequencing data of HNSCC,the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues,which was validated using Real-time RT-PCR and immunohistochemistry.Unexpectedly,overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC.Instead,our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway,leading to enhanced cell proliferation,self-renewal,and resistance to apoptosis.Furthermore,in a patient-derived xenograft(PDX)tumor model,high expression of WNT7A and phosphorylated STAT3 was observed,which positively correlated with tumor progression.These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.

Wnt signaling are critical pathway involved in organ development,tumorigenesis,and cancer progression.WNT7A,a member of the Wnt family,remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma(HNSCC).According to the Cancer Genome Atlas(TCGA),transcriptome sequencing data of HNSCC,the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues,which was validated using Real-time RT-PCR and immunohistochemistry.Unexpectedly,overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC.Instead,our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway,leading to enhanced cell proliferation,self-renewal,and resistance to apoptosis.Furthermore,in a patient-derived xenograft(PDX)tumor model,high expression of WNT7A and phosphorylated STAT3 was observed,which positively correlated with tumor progression.These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.

Wnt signaling are critical pathway involved in organ development,tumorigenesis,and cancer progression.WNT7A,a member of the Wnt family,remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma(HNSCC).According to the Cancer Genome Atlas(TCGA),transcriptome sequencing data of HNSCC,the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues,which was validated using Real-time RT-PCR and immunohistochemistry.Unexpectedly,overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC.Instead,our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway,leading to enhanced cell proliferation,self-renewal,and resistance to apoptosis.Furthermore,in a patient-derived xenograft(PDX)tumor model,high expression of WNT7A and phosphorylated STAT3 was observed,which positively correlated with tumor progression.These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.

Wnt signaling are critical pathway involved in organ development,tumorigenesis,and cancer progression.WNT7A,a member of the Wnt family,remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma(HNSCC).According to the Cancer Genome Atlas(TCGA),transcriptome sequencing data of HNSCC,the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues,which was validated using Real-time RT-PCR and immunohistochemistry.Unexpectedly,overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC.Instead,our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway,leading to enhanced cell proliferation,self-renewal,and resistance to apoptosis.Furthermore,in a patient-derived xenograft(PDX)tumor model,high expression of WNT7A and phosphorylated STAT3 was observed,which positively correlated with tumor progression.These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.

Wnt signaling are critical pathway involved in organ development,tumorigenesis,and cancer progression.WNT7A,a member of the Wnt family,remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma(HNSCC).According to the Cancer Genome Atlas(TCGA),transcriptome sequencing data of HNSCC,the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues,which was validated using Real-time RT-PCR and immunohistochemistry.Unexpectedly,overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC.Instead,our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway,leading to enhanced cell proliferation,self-renewal,and resistance to apoptosis.Furthermore,in a patient-derived xenograft(PDX)tumor model,high expression of WNT7A and phosphorylated STAT3 was observed,which positively correlated with tumor progression.These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.