Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Construction of a risk signature using the least absolute shrinkage and selection operator (LASSO) analysis. Partial likelihood deviances for (A) oesophageal squamous cell carcinoma (ESCC) and (B) oesophageal adenocarcinoma (EAC). Coefficient profiles of senescence‐related gene pairs for (C) ESCC and (D) EAC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques: Selection

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Kaplan–Meier analysis of high‐ and low‐risk patients (red and blue, respectively) with (A) oesophageal squamous cell carcinoma (ESCC) and (B) oesophageal adenocarcinoma (EAC). Receiver operating characteristic curves for (C) ESCC and (D) EAC. Survival risk curves (top) and sand scatter plots (bottom) for (E) ESCC and (F) EAC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Correlations of immune microenvironments evaluated using ESTIMATE. (A) Immune score and (B) ESTIMATE score for oesophageal squamous cell carcinoma (ESCC). (C) Immune score and (D) ESTIMATE score for oesophageal adenocarcinoma (EAC). Relationships between risk and immune scores for (E) ESCC and (H) EAC. Relationships between risk and ESTIMATE scores for (F) ESCC and (G) EAC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Random forest error rates (left graphs) and relative importance (right graphs) for (A) oesophageal squamous cell carcinoma (ESCC) and (B) oesophageal adenocarcinoma (EAC). Expression of IRF5 and BMI1 in (C) ESCC, (D) EAC and (E) EC.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques: Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Multi‐Omics Analysis of Aberrances and Functional Implications of IRF5 in Digestive Tract Tumours

doi: 10.1111/jcmm.70433

Figure Lengend Snippet: Expression analyses of IRF5 in four ESCC cell lines using western blotting (A, B). The efficiency of IRF5 ‐knockdown in KYSE150 cells was determined using western blotting (C, D). Ctrl: No siRNA infection; NC: Negative control. Statistical analyses of n = 3 independent experiments were assessed. Results are shown as mean ± SD, ns p ≥ 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Human ESCC cell lines (KYSE150, KYSE180, KYSE410 and KYSE450) and the human embryonic oesophageal cell line (SHEE) were purchased from iCell Bioscience Inc. (Shanghai, China).

Techniques: Expressing, Western Blot, Knockdown, Infection, Negative Control

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: High QSOX2 enhances stemness, resulting in poor prognosis in ESCC. A) Heat maps showed that QSOX2 was significantly upregulated in ESCC tumors compared to normal esophageal tissues. B) Western blot was used to assess the protein level of QSOX2 in five pairs of ESCC tumors (E) and adjacent normal tissues (N). β‐Tubulin was used as a control. C) IHC staining was employed to analyze the protein level of QSOX2 in adjacent normal tissues, ESCC tumors, and metastatic lymph nodes. D) Kaplan–Meier survival curves demonstrated that a high level of QSOX2 was associated with poor prognosis in ESCC patients. E) Western blot was used to assess the protein level of QSOX2 in immortalized esophageal epithelial cell HET‐1A and six ESCC cell lines. F) Western blot was performed to confirm the overexpression or silence of QSOX2 in ESCC cells. G, H) Western blot was used to detect the expression of stemness markers after QSOX2 overexpression or knockdown. I, J) Flow Cytometry was conducted to measure the level of CD271 in ESCC cells after QSOX2 overexpression or silence. MFI, Mean Fluorescence Intensity. K) Tumor incidence was evaluated in BALB/c‐nude mice one month after injection of ESCC cells with a gradient cell count. L, M) Sphere formation assay was performed to assess the stemness of ESCC cells following QSOX2 overexpression or knockdown. In all panels, data are presented as the mean ± SD; In panels B and C, data were analyzed using paired two‐tailed Student's t‐test with Welch's correction; In panels I‐M, data were analyzed using unpaired two‐tailed Student's t‐test with Welch's correction; * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Control, Immunohistochemistry, Over Expression, Expressing, Knockdown, Flow Cytometry, Fluorescence, Injection, Cell Counting, Tube Formation Assay, Two Tailed Test

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: QSOX2 promotes chemoresistance, proliferation, and metastasis in ESCC cells. A) Cell apoptosis assays evaluated the chemosensitivity of ESCC cells with QSOX2 overexpression. B) Calcein AM/PI double staining was performed to test the apoptotic cell rate of QSOX2 overexpressed ESCC cells under treatments with Cisplatin or Paclitaxel. C) Cell apoptosis assays showed the increased chemosensitivity of ESCC cells with QSOX2 silence. D) Calcein AM/PI double staining was used to analyze the apoptotic cell rate of QSOX2‐silenced ESCC cells treated with Cisplatin or Paclitaxel. E) Co‐expression analysis between QSOX2 and MKI67 in ESCA using the TCGA cohort. F, G) EdU staining was performed to test the cell proliferation rate of ESCC cells with QSOX2 overexpression or silence. H) Xenograft tumor experiment was performed using KYSE510‐Vector and KYSE510‐QSOX2 cells, and tumor volume was calculated. I, J) IHC staining with antibodies against QSOX2 and Ki67 was performed on xenograft tumors derived from QSOX2‐overexpressed KYSE510 cells (I) or QSOX2‐silenced KYSE180 cells (J). K) Transwell assay showed the enhanced cell migration and invasion abilities of ESCC cells with QSOX2 overexpression. L) A lung metastasis experiment was performed to analyze the metastatic ability of KYSE510‐Vector and KYSE510‐QSOX2. In I and J panels, data are presented as the mean ± SEM; other panels, data are presented as the mean ± SD; unpaired two‐tailed Student's t‐test with Welch's correction; * p < 0.05, ** p < 0.01, and *** p < 0.001. ns, no significant difference.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Over Expression, Double Staining, Expressing, Staining, Plasmid Preparation, Immunohistochemistry, Derivative Assay, Transwell Assay, Migration, Two Tailed Test

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: QSOX2 enhances tumor stemness by upregulating c‐Myc. A) Correlation between QSOX2 and MsigDB hallmark gene sets in the TCGA cohort. B) Co‐expression analysis between QSOX2 and cell stemness markers in ESCA using the TCGA cohort. C) Volcano plots illustrate the differentially expressed genes between QSOX2 + and QSOX2 − ESCC cell populations using the GEO dataset ( GSE188955 ). D) Quantification of c‐Myc and QSOX2 staining intensity in ESCC patient tissues ( n = 200 cells) using ImageJ software, followed by linear regression analysis. E) Western blot analysis of c‐Myc expression after QSOX2 overexpression in ESCC cells. F) Percentage of c‐Myc positive tumor cells in xenograft tumors derived from QSOX2‐ or vector‐transfected KYSE510 cells was analyzed by multiplex IF staining. G) Xenograft tumors derived from KYSE510‐QSOX2 cells were treated with Ebselen (5 mg kg −1 , i.p.) every three days for three times 12 days after cell injection, and tumor volume and weight were measured. H) Double IF staining with antibodies against QSOX2 and c‐Myc was performed on KYSE510‐QSOX2‐derived xenograft tumors after treatment with Ebselen. In F and H panels, data are presented as the mean ± SEM; in panel G, data are presented as the mean ± SD; unpaired two‐tailed Student's t‐test with Welch's correction; ** p < 0.01, and *** p < 0.001.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Expressing, Staining, Software, Western Blot, Over Expression, Derivative Assay, Plasmid Preparation, Transfection, Multiplex Assay, Injection, Two Tailed Test

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: QSOX2 activates the mTOR/c‐Myc signaling by promoting the phosphorylation of TSC2 at Ser939 site. A) LC‐MS/MS analysis of QSOX2 binding proteins. B) Protein IP assay was performed with QSOX2 antibody on KYSE30 and KYSE180 cells. C) Multiplex IF staining showed co‐localization of QSOX2, TSC1, and TSC2 in KYSE30 and KYSE180 cells. D) Multiplex IF staining showed co‐localization of QSOX2, TSC1, and TSC2 in ESCC patient tissues. E) Western blot was used to analyze the activation or inactivation of TSC2/mTOR/4E‐BP1/c‐Myc signaling after QSOX2 overexpression or silence in ESCC cells. F) The levels of QSOX2, phosphorylated TSC2 (p‐TSC2 Ser939 ), and phosphorylated mTOR (p‐mTOR Ser2448 ) in ESCC patient tissues with high or low QSOX2 expression were analyzed by multiplex IF staining. G) Multiplex IF staining showed the co‐expression of QSOX2, p‐mTOR Ser2448 and c‐Myc in ESCC patient tissues. H) Multiplex IF staining showed the levels of QSOX2, p‐TSC2 Ser939 , p‐mTOR Ser2448 and c‐Myc in xenograft tumors. I) Western blot was performed to test the levels of p‐mTOR Ser2448 and c‐Myc in KYSE140‐Vector and KYSE140‐QSOX2 cells treated with different concentrations of Rapamycin (24 h). J) Sphere formation assay to evaluate stemness in QSOX2‐overexpressing ESCC cells treated with Rapamycin (10 µM, 24 h). K) Calcein AM/PI double staining was performed to analyze the effect of Rapamycin on the apoptotic cell rate of KYSE140‐Vector and KYSE140‐QSOX2 cells treated with Cisplatin or Paclitaxel. In J and K panels, data are presented as the mean ± SD; unpaired two‐tailed Student's t‐test with Welch's correction; *** p < 0.001. ns, no significant difference.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Phospho-proteomics, Liquid Chromatography with Mass Spectroscopy, Binding Assay, Multiplex Assay, Staining, Western Blot, Activation Assay, Over Expression, Expressing, Plasmid Preparation, Tube Formation Assay, Double Staining, Two Tailed Test

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: QSOX2 promotes disulfide bond formation and phosphorylation of TSC2 by binding Akt. A) Western blot analysis confirming the activation of p‐TSC2 Ser939 after QSOX2 overexpression and the inhibition of p‐TSC2 Ser939 by Akt inhibitor MK‐2206 treatment (5 µM, 24 h). B, C) Western blot analysis showing the effect of QSOX2 on the protein levels of total Akt and p‐Akt Ser473 in the indicated ESCC cells. D) Protein IP assay was performed with TSC2 antibody on ESCC cells with or without QSOX2 overexpression. E) Protein IP assay was performed with TSC2 antibody on ESCC cells with or without QSOX2 silence. F) Multiplex IF demonstrated co‐localization of TSC2, Akt, and QSOX2 in KYSE140‐Vector and KYSE140‐QSOX2 cells. G) Western blot showed the protein band location of TSC2 from Vector‐ or QSOX2‐transfected ESCC cells. Protein lysates were treated with polyethylene glycol maleimide (PEG‐mal) or N‐ethylmaleimide (NEM) as indicated above each blot. PEG‐mal can alkylate free cysteine residues that have not formed disulfide bonds, thereby increasing the molecular weight of the protein. H) ESCC cells were treated with Akt inhibitor MK‐2206 (5 µM, 24 h), and protein lysates were treated with PEG‐mal as indicated above each blot. Western blot analyzed the protein band location of TSC2 from Vector‐ or QSOX2‐transfected ESCC cells. I, J) Mass spectrometry analysis coupled with quantitative bar chart visualization revealed alterations in the disulfide bond formation between C189 and C977/C1026 residues of TSC2 protein in KYSE510‐Vector versus KYSE510‐QSOX2 cells.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Phospho-proteomics, Binding Assay, Western Blot, Activation Assay, Over Expression, Inhibition, Multiplex Assay, Plasmid Preparation, Transfection, Molecular Weight, Mass Spectrometry

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: CAFs‐secreted IGF‐1 upregulates the Akt/mTOR/c‐Myc/QSOX2 signaling. A) CAFs‐conditioned media upregulated the levels of QSOX2, p‐mTOR, p‐4E‐BP1, and c‐Myc in KYSE180 cells. B) Western blot was used to test the levels of QSOX2, p‐mTOR, p‐4E‐BP1, and c‐Myc in KYSE180 cells treated with fibroblasts‐conditioned media. NFs, normal fibroblasts; CAFs, cancer‐associated fibroblasts. C) Multiplex IF staining confirmed that CAFs (α‐SMA positive) were adjacent to QSOX2‐expressed ESCC cells. D) Single‐cell RNA sequencing from GEO datasets ( GSE160269 and GSE188955 ) was performed to identify the main cell populations expressing IGF‐1. E) The levels of QSOX2, p‐mTOR, p‐4E‐BP1, and c‐Myc in KYSE180 cells treated with different concentrations of IGF‐1 (24 h) were analyzed by western blot. F) Western blot confirmed the activation of IGF1R/Akt/mTOR/c‐Myc/QSOX2 signaling in KYSE180 cells by CAFs‐conditioned media, and this stimulation was inhibited by IGF1R inhibitor Linsitinib (5 µM, 24 h). G) Western blot showed the activation of IGF1R/AKT/mTOR/c‐Myc/QSOX2 signaling by IGF‐1 treatment (10 ng µL −1 , 24 h), and this stimulation was inhibited by Linsitinib (5 µM), MK‐2206 (5 µM), or Rapamycin (10 µM). H, I) Multiplex IF staining confirmed the activation of IGF1R/c‐Myc/QSOX2 signaling by IGF‐1 treatment (10 ng µL −1 , 24 h), and this stimulation was inhibited by Linsitinib (5 µM) in KYSE180 (H) and KYSE140 (I) cells. J) The transcriptional binding site of c‐Myc in the QSOX2 gene promoter. K) ChIP‐qPCR analysis showing that IGF‐1 (10 ng µL −1 , 24 h) stimulation promoted the binding of c‐Myc to the promoter of QSOX2 gene. L) Multiplex IF staining was performed to analyze the levels of p‐IGF1R, c‐Myc and QSOX2 on KYSE180‐derived xenograft tumors treated with or without Linstinib (25 mg kg −1 , i.g.). In panel K, data are presented as the mean ± SD; unpaired two‐tailed Student's t‐test with Welch's correction; * p < 0.05.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Multiplex Assay, Staining, RNA Sequencing, Expressing, Activation Assay, Binding Assay, ChIP-qPCR, Derivative Assay, Two Tailed Test

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: Combining Ebselen, Rapamycin, and Cisplatin inhibits ESCC progression. A) Western blot confirmed that the inhibition of mTOR/4E‐BP1/c‐Myc signaling in KYSE140/KYSE510‐QSOX2 cells by Ebselen (100 µM, 24 h) or/and Rapamycin (10 µM, 24 h) treatments. B) Calcein AM/PI double staining was performed to test the apoptotic cell rate of KYSE140‐QSOX2 cells treated with Ebselen (100 µM, 24 h) or/and Rapamycin (10 µM, 24 h). C) Cell apoptosis assays showed the sensitivity of KYSE510‐QSOX2 cells to Ebselen (100 µM, 24 h), Rapamycin (10 µM, 24 h), Cisplatin (10 µM, 24 h), or their combination. D, E) Tumors were generated by s.c. injection of KYSE510‐QSOX2 cells (3 × 10 6 cells per mouse). The mice were treated with Ebselen (5 mg kg −1 , i.p.), Rapamycin (5 mg kg −1 , i.p.), Cisplatin (5 mg kg −1 , i.p.) alone or in combination every three days for three times. Concurrently with the treatment, tumor volume was measured. F) Double IF staining showed the percentage of Ki67 or cleaved Caspase‐3 (Cl‐Casp3) positive tumor cells in KYSE510‐QSOX2‐derived xenograft tumors. G) Double IF staining was performed to analyze the percentage of c‐Myc positive tumor cells in KYSE510‐QSOX2‐derived xenograft tumors treated with the indicated treatments. H) Multiplex IF staining showed the mean fluorescence intensity of p‐p38 and p‐ERK in KYSE510‐QSOX2‐derived xenograft tumors after treatments. In B, C, and E panels, data are presented as the mean ± SD; In panels F‐H, data are presented as the mean ± SEM; unpaired two‐tailed Student's t‐test with Welch's correction; * p < 0.05, ** p < 0.01, and *** p < 0.001. ns, no significant difference.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Inhibition, Double Staining, Generated, Injection, Staining, Derivative Assay, Multiplex Assay, Fluorescence, Two Tailed Test

Journal: Advanced Science

Article Title: QSOX2‐Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c‐Myc Feedback Loop in Esophageal Squamous Cell Carcinoma

doi: 10.1002/advs.202500597

Figure Lengend Snippet: Blocking QSOX2‐mTOR feedback loop, in combination with chemotherapy, reduces tumor stemness and induces tumor dormancy. CAFs secrete IGF‐1 to activate the IGF1R/Akt/mTOR/c‐Myc signaling axis in ESCC cells, leading to an increase in QSOX2 expression. High QSOX2 facilitates the formation of disulfide bonds in TSC2, thereby promoting the binding of TSC2 to Akt and subsequent phosphorylation of TSC2 at the Ser939 site. Phosphorylation of TSC2 at Ser939 relieves its inhibitory effect on mTOR/c‐Myc signaling. Therefore, this mechanism constitutes a positive feedback loop, enhancing tumor stemness, chemotherapy drug resistance, and metastasis of ESCC cells. Inhibiting QSOX2 with Ebselen, in combination with Rapamycin and chemotherapy, inhibits ESCC progression by blocking QSOX2‐mTOR feedback loop, suppressing tumor stemness, enhancing chemotherapy sensitivity, and promoting tumor dormancy.

Article Snippet: The human immortalized esophageal epithelial cell line (HET‐1A) and six ESCC cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) were purchased from the DSMZ (Braunschweig, Germany).

Techniques: Blocking Assay, Expressing, Binding Assay, Phospho-proteomics

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA Expression Profiles in Superficial Esophageal Squamous Cell Carcinoma before Endoscopic Submucosal Dissection: A Pilot Study

doi: 10.3390/ijms22094789

Figure Lengend Snippet: Unsupervised hierarchical clustering analysis of differentially expressed miRNAs between superficial esophageal squamous cell carcinoma (ESCC) and adjacent normal tissues. Columns represent the patients and rows represent the individual miRNAs. Red and blue indicate high and low expression levels, respectively.

Article Snippet: Five human ESCC cell lines (KYSE-150, KYSE-180, KYSE-850, and KYSE-960) were obtained from the Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan).

Techniques: Expressing

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA Expression Profiles in Superficial Esophageal Squamous Cell Carcinoma before Endoscopic Submucosal Dissection: A Pilot Study

doi: 10.3390/ijms22094789

Figure Lengend Snippet: Summary of significantly upregulated and downregulated miRNAs between superficial esophageal squamous cell carcinoma (ESCC) tumor and adjacent (non-tumor) tissues. Fold change (FC) > 2.0, FC < 0.5, p -value < 0.05.

Article Snippet: Five human ESCC cell lines (KYSE-150, KYSE-180, KYSE-850, and KYSE-960) were obtained from the Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan).

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA Expression Profiles in Superficial Esophageal Squamous Cell Carcinoma before Endoscopic Submucosal Dissection: A Pilot Study

doi: 10.3390/ijms22094789

Figure Lengend Snippet: Unsupervised hierarchical clustering analysis of differentially expressed miRNAs in ESCC tissue according to invasion depth and lymphovascular invasion. ( A ) Patients were assigned to two groups based on depth of invasion (cluster A): epithelium (EP, n = 5) or lamina propria, muscularis mucosae, or submucosa (LP/MM/SM1, n = 5). See text for details. ( B ) Patients were assigned to two groups based on the presence ( n = 2) or absence ( n = 8) of lymphovascular invasion (Cluster B). Columns represent the patients and rows represent the individual miRNAs. Red and blue indicate high and low miRNA expression levels, respectively.

Article Snippet: Five human ESCC cell lines (KYSE-150, KYSE-180, KYSE-850, and KYSE-960) were obtained from the Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan).

Techniques: Expressing

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA Expression Profiles in Superficial Esophageal Squamous Cell Carcinoma before Endoscopic Submucosal Dissection: A Pilot Study

doi: 10.3390/ijms22094789

Figure Lengend Snippet: Validation of differential expression of miRNAs in ESCC tissues and cell lines. ( A , B ) qRT-PCR analysis of mi-21-5p, miR-210-3p, and miR-146b-5p in ( A ) 10 matched pairs of superficial ESCC compared with normal tissues (CON), and ( B ) ESCC cell lines compared with normal esophageal epithelial cells (Het-1A). ESCC cells were transfected with a control RNA or miR-21-5p, miR-210-3p, and miR-146b-5p mimics or inhibitors and analyzed in cell counting kit-8 (CCK-8) proliferations assays ( C ) or Transwell invasion and migration assays ( D ). Data are presented as the mean ± standard deviation of triplicates. * p < 0.05, ** p < 0.01 vs. control group.

Article Snippet: Five human ESCC cell lines (KYSE-150, KYSE-180, KYSE-850, and KYSE-960) were obtained from the Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan).

Techniques: Biomarker Discovery, Quantitative Proteomics, Quantitative RT-PCR, Transfection, Control, Cell Counting, CCK-8 Assay, Migration, Standard Deviation

Journal: Journal of Extracellular Vesicles

Article Title: Extracellular vesicles derived from oesophageal cancer containing P4HB promote muscle wasting via regulating PHGDH/Bcl‐2/caspase‐3 pathway

doi: 10.1002/jev2.12060

Figure Lengend Snippet: Development of an ESCC‐induced cachexia mouse model. (a) Body weight analysis of xenograft‐bearing Balb/c nude mice subcutaneously implanted with YES2 (n = 5), KYSE30 (n = 5), KYSE150 (n = 5) and KYSE180 (n = 5) and of respective non‐tumour‐bearing control (Con) mice. (b) GA muscle weight analysis of xenograft‐bearing Balb/c nude mice. (c) Mouse images (left) and body weight changes (right) of xenograft‐bearing Balb/c nude mice subcutaneously implanted with YES2 cells (n = 5) and of respective non‐tumour‐bearing control (Con; n = 5) mice. Mouse images were taken at 8 weeks after YES2 injection. (d) GA muscle images (left) and muscle weight analysis in xenograft‐bearing Balb/c nude mice (n = 5) and non‐ tumour ‐bearing control (Con; n = 5) mice. (e) Representative micrographs of H&E histology of GA muscle in YES2‐bearing mice, relative to non‐tumour‐bearing control mice (n = 5). Scale bars, 150 μm. (f) Quantification of the myofiber cross‐sectional areas in YES2‐bearing mice versus non‐bearing mice. (g) mRNA expression of muscle atrophy markers, MAFbx, MURF1 and Myod1, in GA muscle. n = 7 for Con mice and n = 7 mice for YES2‐bearing mice. (h) Western blot of MURF1 protein in GA muscle from non‐tumour‐bearing control mice (n = 7) and YES2‐bearing mice (n = 7). (i) The apoptosis of GA muscle in YES2‐bearing mice (n = 5), relative to non‐tumour‐bearing control mice (n = 5), was measured by terminal TUNEL assay and quantification of percentage of TUNEL positive cells. Scale bars, 100 μm. (j) Western blot analysis of cleaved caspase‐3 protein and pro caspase‐3 protein in GA muscle from non‐ tumour ‐bearing control mice (n = 6) and YES2‐bearing mice (n = 6)

Article Snippet: Ten human ESCC cell lines, including YES2, KYSE30, KYSE70, KYSE140, KYSE180, KYSE410, KYSE450, KYSE510, COLO680N, were examined in this study, which were kindly provided by Professor Yutaka Shimada from Kyoto University, Japan.

Techniques: Control, Injection, Expressing, Western Blot, TUNEL Assay

Journal: Journal of Extracellular Vesicles

Article Title: Extracellular vesicles derived from oesophageal cancer containing P4HB promote muscle wasting via regulating PHGDH/Bcl‐2/caspase‐3 pathway

doi: 10.1002/jev2.12060

Figure Lengend Snippet: Identification and characterization of EVs derived from ESCC. (a) Representative transmission electron microscopy image of ESCC cell line‐derived EVs (YES2, KYSE30, KYSE150 and KYSE180). (b) Nanoparticle tracking analysis (NTA) indicated the size distribution and concentration of EVs secreted by YES2 cells. (c) Western blot showed expression of EV markers (ALIX, FLOT‐1, and TSG101) in the whole cell lysates and EVs derived from YES2, KYSE30, KYSE150 and KYSE180 cells. LAMIN A/C, albumin and β‐actin were used as non‐exosomal markers. The amount of EVs and cells loaded was normalized to the amount of total proteins. (d) Confocal microscopy images of the internalization of YES2 EVs labelled with 2 nM PKH67 dye in C2C12 myoblasts. Dye alone group was used as a positive control. Untreated control group was used as a negative control. Scale bars, 30 μm. (e) For apoptosis analysis, C2C12 myoblasts were treated with NE2, NE3, YES2, KYSE150 and KYSE180 EVs (10 μg) for 24 h. The cells were collected and stained with annexin V and PI

Article Snippet: Ten human ESCC cell lines, including YES2, KYSE30, KYSE70, KYSE140, KYSE180, KYSE410, KYSE450, KYSE510, COLO680N, were examined in this study, which were kindly provided by Professor Yutaka Shimada from Kyoto University, Japan.

Techniques: Derivative Assay, Transmission Assay, Electron Microscopy, Concentration Assay, Western Blot, Expressing, Confocal Microscopy, Positive Control, Control, Negative Control, Staining

Journal: International Journal of Molecular Sciences

Article Title: Telmisartan Inhibits Cell Proliferation and Tumor Growth of Esophageal Squamous Cell Carcinoma by Inducing S-Phase Arrest In Vitro and In Vivo

doi: 10.3390/ijms20133197

Figure Lengend Snippet: Effects of telmisartan on proliferation of ESCC cell lines in vitro. Telmisartan inhibited proliferation of ESCC cells. Viability of treated cells differed significantly from that of control cells. ( a ) KYSE150, KYSE180, and KYSE850 cells were seeded in 96-well plate (1.0 × 10 4 cells/well). After 24 h, telmisartan (10, 50, or 100 µM) or DMSO were added to the fresh culture medium. Cell viability was assayed daily from 0 to 48 h. ( b ) Cell viability of ESCC cells at 48 h. (* p < 0.01).

Article Snippet: We used three human ESCC cell lines, KYSE150 (Lot.12112008), KYSE180 (Lot.8012008), KYSE850 (Lot.8252001), which were obtained from Japanese Collection of Research Bioresources Cell Bank (Osaka, Japan) on 28 May 2013.

Techniques: In Vitro, Control