human esophageal epithelial cell heec  (Procell Inc)

Journal: Cancer Medicine

Article Title: The GNL3L ‐ MDM2 Interaction Drives Esophageal Squamous Cell Carcinoma Progression

doi: 10.1002/cam4.71146

Figure Lengend Snippet: Expression of GNL3L in esophageal cancer (EC) and the cell line model of GNL3L knockdown. (a) GNL3L expression was analyzed in EC tumor tissues ( n = 182) and normal esophageal tissues ( n = 286) using the GEPIA database. (b) Kaplan–Meier analysis of survival rates between patients with EC and low expression of GNL3L ( n = 138) vs. high expression of GNL3L ( n = 46). In addition to the expression of GNL3L , the survival rate was also related to tumor grade. The patient cohort was obtained from the gene information of TCGA Esophageal cancer datasets downloaded from the UALCAN website. (c) Immunohistochemistry was performed to detect differential expression of GNL3L protein in an esophageal squamous cell carcinoma (ESCC) specimen. (d) qRT‐PCR was used to detect GNL3L expression in ESCC cell lines (TE‐1, KYSE‐410, KYSE‐30, and EC9706) and human normal esophageal epithelial cell line (HEEC). (e) The expression of GNL3L protein in ESCC cell lines and HEEC was assessed using western blotting (WB). (f) Efficiency of sh‐GNL3L for GNL3L in TE‐1 cells by qRT‐PCR. (g) The protein expression of GNL3L in TE‐1 cells. (NC: Negative control). (* p < 0.05, ** p < 0.01).

Article Snippet: ESCC (TE‐1, KYSE‐410, KYSE‐30, EC9706, and ECA‐109) and human normal esophageal epithelial (HEEC) cell lines were obtained from Procell Life Science &Technology Co. Ltd. (Wuhan, China).

Techniques: Expressing, Knockdown, Immunohistochemistry, Quantitative Proteomics, Quantitative RT-PCR, Western Blot, Negative Control

Journal: Journal of Cancer

Article Title: Identification and Characterization of Oxidative Stress and Endoplasmic Reticulum Stress-Related Genes in Esophageal Cancer

doi: 10.7150/jca.104376

Figure Lengend Snippet: TFRC promotes the proliferation, migration, and invasion of ESCA cells. A TFRC expression levels were analyzed in ESCA cells and HEEC using qRT-PCR. B The transfection efficiency of TFRC overexpression in TE1 cells and knockdown in OE33 cells was confirmed by qRT-PCR. C-D Cell proliferation was evaluated in TFRC-overexpressing TE1 cells and TFRC-knockdown OE33 cells using MTS assays (C) and colony formation assays (D). E-F The migration and invasion capabilities of TFRC-overexpressing TE1 cells and TFRC-knockdown OE33 cells were assessed through transwell migration (E) and invasion (F) assays. Data are presented as the mean ± SD from at least three independent experiments. *P < 0.05.

Article Snippet: Human ESCC cell lines (KYSE150 and TE1), an EAC cell line (OE33), and a human normal esophageal epithelial cell line (HEEC) were obtained from the China Center for Type Culture Collection (CCTCC, Wuhan, China).

Techniques: Migration, Expressing, Quantitative RT-PCR, Transfection, Over Expression, Knockdown

Journal: Thoracic Cancer

Article Title: circ‐ TTC17 Promotes Esophagus Squamous Cell Carcinoma Cell Growth, Metastasis, and Inhibits Autophagy‐Mediated Radiosensitivity Through miR ‐145‐5p/ SIRT1 Axis

doi: 10.1111/1759-7714.15494

Figure Lengend Snippet: The expression of circ‐TTC17 and miR‐145‐5p in ESCC. (A–B) QRT‐PCR results indicated that circ‐TTC17 was highly expressed in ESCC tissues (T) and cell lines compared with that in adjacent normal tissues (N) and HEEC cells, respectively. * p < 0.05.

Article Snippet: ESCC cell lines (TE1, KYSE150, KYSE180, and KYSE30) and human esophageal epithelial cells (HEEC) were purchased from Procell (Wuhan, China) and grown in RPMI‐1640 medium containing 10% FBS and 1% penicillin/streptomycin. circ‐TTC17 siRNA, lentiviral shRNA, miR‐145‐5p mimic, anti‐miR‐145‐5p, and negative controls were transfected into KYSE180 and KYSE30 cells by Lipofectamine 3000 (Invitrogen, Carlsbad, CA, USA).

Techniques: Expressing, Quantitative RT-PCR

Journal: Thoracic Cancer

Article Title: circ‐ TTC17 Promotes Esophagus Squamous Cell Carcinoma Cell Growth, Metastasis, and Inhibits Autophagy‐Mediated Radiosensitivity Through miR ‐145‐5p/ SIRT1 Axis

doi: 10.1111/1759-7714.15494

Figure Lengend Snippet: miR‐145‐5p targeted SIRT1 in ESCC. (A) The binding sequences between miR‐145‐5p and SIRT1 3′UTR were presented. The interaction was verified using dual‐luciferase reporter assay (B–C) and RIP assay (D–E). (F) QRT‐PCR was used to detect SIRT1 mRNA expression in ESCC tissues (T) and adjacent normal tissues (N). (G) The correlation between SIRT1 and miR‐145‐5p expression was assessed by Pearson correlation coefficient analysis. (H) The protein expression of SIRT1 in T and N was determined by WB analysis. The mRNA and protein levels of SIRT1 in ESCC cell lines and HEEC cells were measured using qRT‐PCR (I) and WB analysis (J), respectively. (K) The transfection efficiency of miR‐145‐5p mimic and inhibitor was evaluated using qRT‐PCR. (L) SIRT1 protein expression in KYSE180 and KYSE30 cells was determined by WB analysis. * p < 0.05.

Article Snippet: ESCC cell lines (TE1, KYSE150, KYSE180, and KYSE30) and human esophageal epithelial cells (HEEC) were purchased from Procell (Wuhan, China) and grown in RPMI‐1640 medium containing 10% FBS and 1% penicillin/streptomycin. circ‐TTC17 siRNA, lentiviral shRNA, miR‐145‐5p mimic, anti‐miR‐145‐5p, and negative controls were transfected into KYSE180 and KYSE30 cells by Lipofectamine 3000 (Invitrogen, Carlsbad, CA, USA).

Techniques: Binding Assay, Luciferase, Reporter Assay, Quantitative RT-PCR, Expressing, Transfection