Journal: Molecular medicine reports

Article Title: MEK inhibitor enhanced the antitumor effect of oxaliplatin and 5‑fluorouracil in MEK1 Q56P‑mutant colorectal cancer cells.

doi: 10.3892/mmr.2018.9730

Figure Lengend Snippet: Figure 4. Gene expression induced by U0126 combined with or without oxaliplatin/5‑FU. (A) ERCC1 mRNA levels in SW48 cells were examined by RT‑qPCR following treatment with U0126 and/or oxaliplatin. (B) TYMS mRNA levels in SW48 cells were examined by RT‑qPCR following treatment with U0126 and/or 5‑FU. The graph depicts the fold change in ERCC1/TYMS levels normalized to β‑actin levels. Data are presented as means ± standard deviation. Western blot analysis results of (C) ERCC1 and (D) TYMS protein expression levels in cells treated with U0126 in combination with oxaliplatin or 5‑FU, respectively. **P<0.01 vs. control group; ##P<0.01 vs. oxaliplatin/5‑FU‑treated group. 5‑FU, 5‑fluorouracil; ERCC1, excision repair cross‑complementation group 1; TYMS, thymidylate synthase; RT‑qPCR, reverse transcription‑quantitative polymerase chain reaction.

Article Snippet: Excision repair cross-complementation group 1 (ERCC1) rabbit polyclonal antibody (cat. no. 14586‐1‐AP) and TYMS rabbit polyclonal antibody (cat. no. 15047‐1‐AP) were purchased from ProteinTech Group, Inc. (Wuhan, China).

Techniques: Gene Expression, Standard Deviation, Western Blot, Expressing, Control, Polymerase Chain Reaction

Journal: Experimental and Therapeutic Medicine

Article Title: Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models

doi: 10.3892/etm.2018.6299

Figure Lengend Snippet: LaCl 3 and cisplatin co-treatment altered the expression levels of tumor-associated proteins in COC1 cells. Expression levels of (A) Ki67, (B) BCL-2, (C) BRCA1, (D) BRCA2, and (E) ERCC1 are demonstrated. Ki67 expression decreased in the presence of cisplatin compared with the control, while application of cisplatin + LaCl 3 further decreased Ki67 expression, and LaCl 3 alone had only a minor effect. Similar results were obtained for BCL-2 and ERCC1 expression levels. By contrast, cisplatin increased the expression levels of BRCA1 and BRCA2 compared with the control cells, while co-application of LaCl 3 and cisplatin further increased the levels, and LaCl 3 alone did not have a marked effect. Scale bar, 20 µm. Magnification, ×200. LaCl 3 , lanthanum chloride; BCL-2, B-cell lymphoma-2; BRCA, breast cancer; ERCC1, excision repair cross-complementation group 1.

Article Snippet: Next, samples were incubated overnight at 4°C with primary antibodies against: B-cell lymphoma-2 (BCL-2; cat. no. ab692; 1:500), Ki67 (cat. no. ab15580, 1:500), breast cancer 1 (BRCA1; cat. no. ab16780; 1:500), BRCA2 (cat. no. ab27976; 1:500) and excision repair cross-complementation group 1 (ERCC1; cat. no. ab2356; 1:100; all purchased from Abcam, Cambridge, UK).

Techniques: Expressing

Journal: Experimental and Therapeutic Medicine

Article Title: Effect of lanthanum chloride on tumor growth and apoptosis in human ovarian cancer cells and xenograft animal models

doi: 10.3892/etm.2018.6299

Figure Lengend Snippet: Co-treatment with LaCl 3 with cisplatin altered the expression levels of (A) Ki67, (B) BCL-2, (C) BRCA1, (D) BRCA2, and (E) ERCC1 in COC1/DPP cells. The effects of different treatments were similar with those in COC1 cells. Scale bar, 20 µm. Magnification, ×200. LaCl 3 , lanthanum chloride; BCL-2, B-cell lymphoma-2; BRCA, breast cancer; ERCC1, excision repair cross-complementation group 1.

Article Snippet: Next, samples were incubated overnight at 4°C with primary antibodies against: B-cell lymphoma-2 (BCL-2; cat. no. ab692; 1:500), Ki67 (cat. no. ab15580, 1:500), breast cancer 1 (BRCA1; cat. no. ab16780; 1:500), BRCA2 (cat. no. ab27976; 1:500) and excision repair cross-complementation group 1 (ERCC1; cat. no. ab2356; 1:100; all purchased from Abcam, Cambridge, UK).

Techniques: Expressing

Journal: Molecular Medicine Reports

Article Title: MEK inhibitor enhanced the antitumor effect of oxaliplatin and 5-fluorouracil in MEK1 Q56P-mutant colorectal cancer cells

doi: 10.3892/mmr.2018.9730

Figure Lengend Snippet: Gene expression induced by U0126 combined with or without oxaliplatin/5-FU. (A) ERCC1 mRNA levels in SW48 cells were examined by RT-qPCR following treatment with U0126 and/or oxaliplatin. (B) TYMS mRNA levels in SW48 cells were examined by RT-qPCR following treatment with U0126 and/or 5-FU. The graph depicts the fold change in ERCC1/TYMS levels normalized to β-actin levels. Data are presented as means ± standard deviation. Western blot analysis results of (C) ERCC1 and (D) TYMS protein expression levels in cells treated with U0126 in combination with oxaliplatin or 5-FU, respectively. **P<0.01 vs. control group; ## P<0.01 vs. oxaliplatin/5-FU-treated group. 5-FU, 5-fluorouracil; ERCC1, excision repair cross-complementation group 1; TYMS, thymidylate synthase; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.

Article Snippet: Excision repair cross-complementation group 1 (ERCC1) rabbit polyclonal antibody (cat. no. 14586-1-AP) and TYMS rabbit polyclonal antibody (cat. no. 15047-1-AP) were purchased from ProteinTech Group, Inc. (Wuhan, China).

Techniques: Gene Expression, Quantitative RT-PCR, Standard Deviation, Western Blot, Expressing, Control, Reverse Transcription, Real-time Polymerase Chain Reaction

Journal: Cancer Research and Treatment : Official Journal of Korean Cancer Association

Article Title: p21-Activated Kinase 4 (PAK4) as a Predictive Marker of Gemcitabine Sensitivity in Pancreatic Cancer Cell Lines

doi: 10.4143/crt.2014.054

Figure Lengend Snippet: Protein expression of p21-activated kinases (PAKs) and signaling molecules related to gemcitabine sensitivity. An inverse relationship was observed between PAK4 and human equilibrative nucleoside transporter 1 (hENT1) protein expression. (A) In gemcitabine-resistant cell lines (Capan-2, PANC-1, and SNU-410), higher PAK4 and lower hENT1 protein expression are shown. (B) There is no correlation between molecules of the epidermal growth factor receptor (EGFR) pathway (EGFR, p-EGFR, AKT, p-AKT, ERK, and p-ERK) and sensitivity to gemcitabine. The quantitative graph of densitometry (C) shows a significant correlation between PAK4 and hENT1 expression in pancreatic cancer cell lines.

Article Snippet: After blocking with 5% nonfat milk in TBST for 1 hour, the membranes were incubated with the primary antibody to PAK4 (Abcam, Cambridge, MA), human equilibrative nucleoside transporter 1 (hENT1; Proteintech, Chicago, IL), excision repair cross-complementing rodent repair deficiency, complementation group 1 (ERCC1, Santa Cruz Biotech, Santa Cruz, CA), PAK1, phosphorylated epidermal growth factor receptor, EGFR, pAkt, Akt, pErk, Erk, and β-actin (Cell Signaling).

Techniques: Expressing

Journal: Cancer Research and Treatment : Official Journal of Korean Cancer Association

Article Title: p21-Activated Kinase 4 (PAK4) as a Predictive Marker of Gemcitabine Sensitivity in Pancreatic Cancer Cell Lines

doi: 10.4143/crt.2014.054

Figure Lengend Snippet: Protein expression of p21-activated kinases (PAKs) and signaling molecules related to gemcitabine sensitivity. An inverse relationship was observed between PAK4 and human equilibrative nucleoside transporter 1 (hENT1) protein expression. (A) In gemcitabine-resistant cell lines (Capan-2, PANC-1, and SNU-410), higher PAK4 and lower hENT1 protein expression are shown. (B) There is no correlation between molecules of the epidermal growth factor receptor (EGFR) pathway (EGFR, p-EGFR, AKT, p-AKT, ERK, and p-ERK) and sensitivity to gemcitabine. The quantitative graph of densitometry (C) shows a significant correlation between PAK4 and hENT1 expression in pancreatic cancer cell lines.

Article Snippet: After blocking with 5% nonfat milk in TBST for 1 hour, the membranes were incubated with the primary antibody to PAK4 (Abcam, Cambridge, MA), human equilibrative nucleoside transporter 1 (hENT1; Proteintech, Chicago, IL), excision repair cross-complementing rodent repair deficiency, complementation group 1 (ERCC1, Santa Cruz Biotech, Santa Cruz, CA), PAK1, phosphorylated epidermal growth factor receptor, EGFR, pAkt, Akt, pErk, Erk, and β-actin (Cell Signaling).

Techniques: Expressing

Journal: International Journal of Oncology

Article Title: Mechanism of resistance to chemoradiation in p53 mutant human colon cancer

doi: 10.3892/ijo.32.6.1305

Figure Lengend Snippet: Figure 4. Exposure to 5-FU up-regulated EGFR and simultaneously down-regulated ERCC1 expression in radio-resistant SW480 cells. In contrast, exposure to 5-FU down-regulated EGFR and simultaneously up-regulated ERCC1 expression in radio-sensitive cell lines.

Article Snippet: The primary antibodies used were: mouse monoclonal anti- the excision repair cross complementation group 1 (ERCC1) antibody (1:250 dilution; Santa Cruz Biotechnology), a mouse monoclonal anti-EGFR antibody (1:400 dilution; Cell Signaling Technology) and mouse monoclonal anti-actin (clone C4) antibody (1:1000 dilution; ICN Biomedicals, Aurora, OH, USA).

Techniques: Expressing

Journal: International Journal of Oncology

Article Title: Mechanism of resistance to chemoradiation in p53 mutant human colon cancer

doi: 10.3892/ijo.32.6.1305

Figure Lengend Snippet: Figure 5. Alteration of EGFR and ERCC1 proteins during chemoradiation in SW480 cells was apparently inversely related to that in other radiosensitive cell lines. After chemoradiation, up-regulation of EGFR in SW480 was maintained.

Article Snippet: The primary antibodies used were: mouse monoclonal anti- the excision repair cross complementation group 1 (ERCC1) antibody (1:250 dilution; Santa Cruz Biotechnology), a mouse monoclonal anti-EGFR antibody (1:400 dilution; Cell Signaling Technology) and mouse monoclonal anti-actin (clone C4) antibody (1:1000 dilution; ICN Biomedicals, Aurora, OH, USA).

Techniques:

Journal: Biomarkers in Cancer

Article Title: Molecular Profiling of Refractory Adrenocortical Cancers and Predictive Biomarkers to Therapy

doi: 10.4137/BIC.S34292

Figure Lengend Snippet: IHC markers of sensitivity and resistance to current ACC therapy.

Article Snippet: Antibodies used included: androgen receptor (AR), topoisomerases 1 and 2 (TOPO1, TOPO2A, Leica Biosystems), estrogen receptor (ER), progesterone receptor (PR), cMet, human epidermal growth factor receptor 2 (HER2; Ventana), cKIT, epidermal growth factor receptor (EGFR), phosophatase and tensin homolog (PTEN; Dako), O(6)-methylguanine-methyltransferase (MGMT), PGP, thymidylate synthase (TS; Invitrogen), transducin-like enhancer of split 3 (Santa Cruz), excision repair cross complimentary group 1 (ERCC1; Abcam), RRM1 (Proteintech), SPARC (monoclonal; R&D Systems and polyclonal; Exalpha) and tubulin beta-3 chain (Covance), programmed cell death protein 1 (PD-1), and programmed death-ligand 1 (PD-L1; BD Pharmingen and R&D Systems).

Techniques: Marker