Journal: Anticancer research

Article Title: Base Excision Repair Activities Differ in Human Lung Cancer Cells and Corresponding Normal Controls

doi:

Figure Lengend Snippet: Cell lines used.

Article Snippet: The cells were harvested at 80% confluence with trypsin, washed with PBS, and immediately processed for mitochondria and nuclei isolation. table ft1 table-wrap mode="anchored" t5 caption a7 Tumor cell lines Normal cell lines ATCC number (Designation) Cancer type Source Morphology ATCC number (Designation) Source Morphology NCI-H2087 ( CRL-5922 ) Adenocarcinoma; non-small cell lung cancer Lymphonode Epithelial NCI-BL2087 ( CRL-5965 ) Peripheral blood Lymphoblast NCI-H2107 ( CRL-5983 ) Carcinoma, small cell lung cancer Bone marrow Epithelial NCI-BL2107 ( CRL-5966 ) Peripheral blood Lymphoblast NCI-H2052 ( CRL-5915 ) Mesothelioma Pleural effusion – NCI-BL2052 ( CRL-5963 ) Peripheral blood Lymphoblast Open in a separate window Cell lines used.

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Journal: Molecular Oncology

Article Title: Glutathione S ‐transferase omega class 1 ( GSTO1 )‐associated large extracellular vesicles are involved in tumor‐associated macrophage‐mediated cisplatin resistance in bladder cancer

doi: 10.1002/1878-0261.13659

Figure Lengend Snippet: Macrophages increase the resistance of bladder cancer to cisplatin. (A) The correlation between macrophage infiltration and OS in patients with bladder cancer was analyzed by the TIMER2.0 website. (B) The correlation between CD163 expression and OS in patients with bladder cancer was analyzed by the Kaplan–Meier‐plotter cancer database. The high versus low expression levels of CD163 mRNA were split by the upper tertile value. The threshold of follow‐up for patients was set at 60 months. (C) The expression of the CD163 gene in various pathological stages of bladder cancer was analyzed by the pathological stage plot on the GEPIA web server. The expression violin plots were generated using log 2 (TPM + 1) transformed expression data on the patient's pathological stage. (D) Cell viabilities of HT1376 and BFTC905 with or without 20% CM treatment in indicated doses of cisplatin for 24 h were determined by the MTT assay ( n = 3). The data were displayed as the means ± standard deviation (SD). P values were calculated using a two‐tailed unpaired Student's t ‐test (D). ** P < 0.01. CM, condition media; OS, overall survival; TPM, transcripts per million.

Article Snippet: The expression of GSTO1 in human bladder normal tissues and tumor tissues was assessed using a pathological tissue array (#BL2081b) obtained from US Biomax in Derwood, MD, USA.

Techniques: Expressing, Generated, Transformation Assay, MTT Assay, Standard Deviation, Two Tailed Test

Journal: Molecular Oncology

Article Title: Glutathione S ‐transferase omega class 1 ( GSTO1 )‐associated large extracellular vesicles are involved in tumor‐associated macrophage‐mediated cisplatin resistance in bladder cancer

doi: 10.1002/1878-0261.13659

Figure Lengend Snippet: GSTO1 contributes to cisplatin resistance in bladder cancer. (A) The sample description of the pathological tissue array (Cat. No. BL2081b; US Biomax). (B) The expressions of GSTO1 in bladder normal ( n = 16) and cancer tissues ( n = 168) were analyzed using the pathological tissue array. Scale bar = 50 μm. (C) The H ‐score method was used to quantitatively assess the IHC results (normal = 16; cancer = 168). (D) The sample description of bladder cancer patients after cisplatin treatment. (E) The expressions of GSTO1 in high ( n = 5) and low ( n = 8) cisplatin response patients using IHC. Scale bar = 100 μm. (F) The GSTO1 positive area was used to quantitatively assess the IHC results (low response = 8; high response = 5). (G) Cell viabilities of cisplatin‐resistant HT1376 and BFTC905 and their controls at indicated doses of cisplatin for 24 h were determined by the MTT assay ( n = 3). (H) The expression of GSTO1 in cisplatin‐resistant HT1376 and BFTC905 and their controls was determined by western blot assay ( n = 3). β‐Actin, loading control. (I) Cell viability of GSTO1‐OE and the control HT1376 at the indicated doses of cisplatin for 24 h was determined by the MTT assay. GSTO1‐OE in HT1376 was validated by western blot assay (right panel) ( n = 3). (J) Cell viability of GSTO1‐KO and the control HT1376 at the indicated doses of cisplatin for 24 h was determined by the MTT assay. GSTO1‐KO in HT1376 was validated by Western blot assay (right panel) ( n = 3). (K) Cell viabilities of HT1376 with or without GSTO1 inhibitor GSTO1‐IN‐1 (1 μ m ) treatment in indicated doses of cisplatin for 24 h were determined by the MTT assay ( n = 3). The effect of GSTO1‐IN‐1 on GSTO1 expression of HT1376 was determined by Western blot assay (right panel) ( n = 3). (L) Cell viabilities of GSTO1‐KO and the control HT1376 in the presence or absence of CM (20%) in indicated doses of cisplatin for 24 h were determined by the MTT assay ( n = 3). (M) Cell viabilities of GSTO1‐KO and the control HT1376 in the presence or absence of TNF‐α (20 ng·mL −1 ) in indicated doses of cisplatin for 24 h were determined by the MTT assay ( n = 3). Data were displayed as the means ± SEM (C, F) or the mean ± SD (G, I–M). P values were calculated using a two‐tailed, unpaired Student's t ‐test (C, F, G, I–M). * P < 0.05; ** P < 0.01. cisplatin/R, cisplatin resistance; HGUC, high‐grade urothelial carcinoma; IHC, immunohistochemistry; KO, knockout; LGUC, low‐grade urothelial carcinoma; OE, overexpression.

Article Snippet: The expression of GSTO1 in human bladder normal tissues and tumor tissues was assessed using a pathological tissue array (#BL2081b) obtained from US Biomax in Derwood, MD, USA.

Techniques: MTT Assay, Expressing, Western Blot, Control, Two Tailed Test, Immunohistochemistry, Knock-Out, Over Expression