Journal: International Journal of Biological Sciences

Article Title: MG53 inhibits cellular proliferation and tumor progression in colorectal carcinoma

doi: 10.7150/ijbs.67869

Figure Lengend Snippet: Anti-proliferative effects of rhMG53 on parental and ABCB1-overexpressing cells. Cytotoxicity assay was conducted to evaluate the anti-proliferative effects of rhMG53 on parental SW620 and ABCB1-overexpressing SW620/AD300 cells (A) and HCT15 and S1 cells (B). The data are the representation of mean ± SD for three independent experiments performed in triplicates.

Article Snippet: The ABCB1 (E1Y7S) rabbit mAb (catalog number 13978S) and β-Actin (13E5) rabbit mAb (catalog number 4970S) were purchased from Cell Signaling Technology (Danvers, MA) and used at 1:1000 dilutions.

Techniques: Cytotoxicity Assay

Journal: International Journal of Biological Sciences

Article Title: MG53 inhibits cellular proliferation and tumor progression in colorectal carcinoma

doi: 10.7150/ijbs.67869

Figure Lengend Snippet: The effect of rhMG53 on reversal of ABCB1-mediated MDR.

Article Snippet: The ABCB1 (E1Y7S) rabbit mAb (catalog number 13978S) and β-Actin (13E5) rabbit mAb (catalog number 4970S) were purchased from Cell Signaling Technology (Danvers, MA) and used at 1:1000 dilutions.

Techniques:

Journal: International Journal of Biological Sciences

Article Title: MG53 inhibits cellular proliferation and tumor progression in colorectal carcinoma

doi: 10.7150/ijbs.67869

Figure Lengend Snippet: Effect of rhMG53 on the expression of ABCB1. SW620/AD300 cells were treated with rhMG53 at different time points (A) or different concentrations (B). Similar amounts of cell lysates were used, and Western blot analysis was conducted. The band intensity of ABCB1/β-actin was obtained with Image J and labeled as grayscale ratios (C, D). The differences presented are not statistically significant (p > 0.05).

Article Snippet: The ABCB1 (E1Y7S) rabbit mAb (catalog number 13978S) and β-Actin (13E5) rabbit mAb (catalog number 4970S) were purchased from Cell Signaling Technology (Danvers, MA) and used at 1:1000 dilutions.

Techniques: Expressing, Western Blot, Labeling

Journal: Oncology Research

Article Title: The AKT/GSK3β-Mediated Slug Expression Contributes to Oxaliplatin Resistance in Colorectal Cancer via Upregulation of ERCC1

doi: 10.3727/096504020X15877284857868

Figure Lengend Snippet: Antibodies Used in the Study

Article Snippet: ABCB1 , 13978T , Cell Signaling Technology.

Techniques:

Journal: Heliyon

Article Title: The potential effects and mechanisms of Gegen Qinlian Decoction in oxaliplatin-resistant colorectal cancer based on network pharmacology

doi: 10.1016/j.heliyon.2022.e11305

Figure Lengend Snippet: A total of 80 differential genes of CRC drug resistance showing the greatest change.

Article Snippet: Rabbit anti-ABCB1 (#13978), rabbit anti-ABCC2 (#12559), and rabbit anti-ABCG2 (#42078) were purchased from CST (Danvers, MA, USA), and rabbit anti-NA-K-ATPase was purchased from Abbkine (ABP55363).

Techniques:

Journal: Heliyon

Article Title: The potential effects and mechanisms of Gegen Qinlian Decoction in oxaliplatin-resistant colorectal cancer based on network pharmacology

doi: 10.1016/j.heliyon.2022.e11305

Figure Lengend Snippet: Specific binding sites of proteins and active components. 1: ABCB1; 2: ABCG2; A–E: wogonin, baicalein, baicalin, liquiritigenin, oroxylin a.

Article Snippet: Rabbit anti-ABCB1 (#13978), rabbit anti-ABCC2 (#12559), and rabbit anti-ABCG2 (#42078) were purchased from CST (Danvers, MA, USA), and rabbit anti-NA-K-ATPase was purchased from Abbkine (ABP55363).

Techniques: Binding Assay

Journal: Heliyon

Article Title: The potential effects and mechanisms of Gegen Qinlian Decoction in oxaliplatin-resistant colorectal cancer based on network pharmacology

doi: 10.1016/j.heliyon.2022.e11305

Figure Lengend Snippet: Depiction of the specific binding force.

Article Snippet: Rabbit anti-ABCB1 (#13978), rabbit anti-ABCC2 (#12559), and rabbit anti-ABCG2 (#42078) were purchased from CST (Danvers, MA, USA), and rabbit anti-NA-K-ATPase was purchased from Abbkine (ABP55363).

Techniques: Binding Assay

Journal: Heliyon

Article Title: The potential effects and mechanisms of Gegen Qinlian Decoction in oxaliplatin-resistant colorectal cancer based on network pharmacology

doi: 10.1016/j.heliyon.2022.e11305

Figure Lengend Snippet: GQD alone and in synergy with OXA inhibited the protein and mRNA expression of the ABC transporter (A, B) Protein and mRNA expression of ABCB1, ABCC2, and ABCG2 in HCT116 and HCT116/L (C–F) The protein expression and mRNA changes of ABCB1, ABCC2, and ABCG2 when GQD and OXA acted either alone or together for 12 and 24 h. Data are presented as the mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. 2 mg/mL, 2.5 mg/mL: GQD concentration. 100 μM: OXA concentration.

Article Snippet: Rabbit anti-ABCB1 (#13978), rabbit anti-ABCC2 (#12559), and rabbit anti-ABCG2 (#42078) were purchased from CST (Danvers, MA, USA), and rabbit anti-NA-K-ATPase was purchased from Abbkine (ABP55363).

Techniques: Expressing, Concentration Assay

Journal: Frontiers in Oncology

Article Title: Co-administration of MDR1 and BCRP or EGFR/PI3K inhibitors overcomes lenvatinib resistance in hepatocellular carcinoma

doi: 10.3389/fonc.2022.944537

Figure Lengend Snippet: MDR1 and BCRP overexpression and EGFR signalling pathway activation following LR induction. (A–C) qRT-PCR, western blotting, and immunofluorescence analysis demonstrated that MDR1 and BCRP expression was upregulated following LR induction. Scale bars, 100 μm. (D) Western blotting revealed that EGFR and its downstream MEK/ERK and PI3K/AKT pathways were markedly activated following LR induction. ** p < 0.01. *** p < 0.001.

Article Snippet: The cells were then washed thrice with PBS, fixed with 4% paraformaldehyde (PFA) for 20 min, blocked with 10% goat serum, and incubated with primary antibodies MDR1 (Rabbit mAb #13978 CST) and BCRP (Mouse mAb #130244 Abcam) for another day.

Techniques: Over Expression, Activation Assay, Quantitative RT-PCR, Western Blot, Immunofluorescence, Expressing

Journal: Frontiers in Oncology

Article Title: Co-administration of MDR1 and BCRP or EGFR/PI3K inhibitors overcomes lenvatinib resistance in hepatocellular carcinoma

doi: 10.3389/fonc.2022.944537

Figure Lengend Snippet: In vitro combined antitumour effect of lenvatinib and elacridar. (A) Schematic diagram indicates that elacridar dually inhibited MDR1 and BCRP. (B, C) The MTT results and CI plots confirmed that elacridar synergised with lenvatinib to inhibit Huh7 LR cell viability. (D, E) Co-treatment with elacridar and lenvatinib enhanced cell apoptosis, as shown in micrographs and flow cytometry plots. (F, G) Combined elacridar and lenvatinib treatment inhibited colony formation and downregulated CD133, EpCAM, SOX-9, and c-Myc expression. *** p < 0.001.

Article Snippet: The cells were then washed thrice with PBS, fixed with 4% paraformaldehyde (PFA) for 20 min, blocked with 10% goat serum, and incubated with primary antibodies MDR1 (Rabbit mAb #13978 CST) and BCRP (Mouse mAb #130244 Abcam) for another day.

Techniques: In Vitro, Flow Cytometry, Expressing

Journal: Frontiers in Oncology

Article Title: Co-administration of MDR1 and BCRP or EGFR/PI3K inhibitors overcomes lenvatinib resistance in hepatocellular carcinoma

doi: 10.3389/fonc.2022.944537

Figure Lengend Snippet: MDR1 and BCRP overexpression and EGFR signalling pathway activation following LR induction. (A–C) qRT-PCR, western blotting, and immunofluorescence analysis demonstrated that MDR1 and BCRP expression was upregulated following LR induction. Scale bars, 100 μm. (D) Western blotting revealed that EGFR and its downstream MEK/ERK and PI3K/AKT pathways were markedly activated following LR induction. ** p < 0.01. *** p < 0.001.

Article Snippet: Antibodies against total epidermal growth factor receptor (EGFR; A11577, ABclonal), phospho-EGFR (AP0820, ABclonal), total PI3K (ab32089, Abcam), phospho-PI3K (4228, CST), total AKT (9272, CST), phospho-AKT (4060, CST), total MEK1/2 (A4868, ABclonal), phospho-MEK1/2 (AP0209, ABclonal), total ERK1/2 (4695, CST), phospho-ERK1/2 (4376, CST), caspase-3 (T40051, Abmart), Bcl-2-associated X (Bax; T40044, Abmart), multidrug resistance protein 1 (MDR1; 13978, CST), breast cancer resistance protein (BCRP; 130244, Abcam), and glyceraldehyde 3-phosphate dehydrogenase (GAPDH; 5174, CST) were used.

Techniques: Over Expression, Activation Assay, Quantitative RT-PCR, Western Blot, Immunofluorescence, Expressing

Journal: Frontiers in Oncology

Article Title: Co-administration of MDR1 and BCRP or EGFR/PI3K inhibitors overcomes lenvatinib resistance in hepatocellular carcinoma

doi: 10.3389/fonc.2022.944537

Figure Lengend Snippet: In vitro combined antitumour effect of lenvatinib and elacridar. (A) Schematic diagram indicates that elacridar dually inhibited MDR1 and BCRP. (B, C) The MTT results and CI plots confirmed that elacridar synergised with lenvatinib to inhibit Huh7 LR cell viability. (D, E) Co-treatment with elacridar and lenvatinib enhanced cell apoptosis, as shown in micrographs and flow cytometry plots. (F, G) Combined elacridar and lenvatinib treatment inhibited colony formation and downregulated CD133, EpCAM, SOX-9, and c-Myc expression. *** p < 0.001.

Article Snippet: Antibodies against total epidermal growth factor receptor (EGFR; A11577, ABclonal), phospho-EGFR (AP0820, ABclonal), total PI3K (ab32089, Abcam), phospho-PI3K (4228, CST), total AKT (9272, CST), phospho-AKT (4060, CST), total MEK1/2 (A4868, ABclonal), phospho-MEK1/2 (AP0209, ABclonal), total ERK1/2 (4695, CST), phospho-ERK1/2 (4376, CST), caspase-3 (T40051, Abmart), Bcl-2-associated X (Bax; T40044, Abmart), multidrug resistance protein 1 (MDR1; 13978, CST), breast cancer resistance protein (BCRP; 130244, Abcam), and glyceraldehyde 3-phosphate dehydrogenase (GAPDH; 5174, CST) were used.

Techniques: In Vitro, Flow Cytometry, Expressing

Journal: Frontiers in Oncology

Article Title: Glutor, a Glucose Transporter Inhibitor, Exerts Antineoplastic Action on Tumor Cells of Thymic Origin: Implication of Modulated Metabolism, Survival, Oxidative Stress, Mitochondrial Membrane Potential, pH Homeostasis, and Chemosensitivity

doi: 10.3389/fonc.2022.925666

Figure Lengend Snippet: Chemosensitizing action of glutor DL cells (1 × 10 5 ) were incubated in a medium alone or containing glutor (0.01 µM) for 24 h in the presence or absence of cisplatin, followed by estimation of cell survival (A) by MTT assay as described in the Materials and Methods section. Control and glutor-treated DL cells were also evaluated for MDR1 expression (B) by Western blotting. Values in (A) are the mean ± SD. The plates shown in (B) are from a representative experiment out of at least two experiments with similar results. The accompanying bar diagram depicts the densitometry of the bands. *p< 0.05 vs. respective control; p< 0.05 vs. DL cells treated with glutor or cisplatin alone.

Article Snippet: Primary antibodies against GLUT1 (E-AB-31556), GLUT3 (E-AB-31557), HK-2 (E-AB-14706), and LDH-A (E-AB-19937) were purchased from Elabscience USA; HIF1-α (SC-31515), C-myc (SC-40), p53 (SC-126), β-actin (SC-47778), BAX(CST 2772S), Hsp70 (CST 4872S), and MDR1/ABCB1 (CST 13978) were purchased from Cell Signaling Technology (CST) USA; VEGF (IMG-80214), TGF-β (IMG-6667-E-100), Bcl-2 (IMG-3181), and MCT1 (IMG-4021) were purchased from Imagenex, USA; PE-CD25 (55386) was purchased from BD Biosciences, USA.

Techniques: Incubation, MTT Assay, Expressing, Western Blot

Journal: Frontiers in Oncology

Article Title: Lapatinib Suppresses HER2-Overexpressed Cholangiocarcinoma and Overcomes ABCB1– Mediated Gemcitabine Chemoresistance

doi: 10.3389/fonc.2022.860339

Figure Lengend Snippet: Lapatinib suppresses the function of elevated ABCB1 after being treated with gemcitabine in CCA cells. (A) The growth inhibitory effects of gemcitabine (Gem) on FRH-0201 and FRH0201-Gem. (B, C) ABCB1 protein expression in FRH-0201 and FRH0201-Gem was detected with Western blotting and immunofluorescence. Scale bar: 20 μm. (D) Quantification of fluorescence intensity for ABCB1 in FRH-0201, FRH0201-Gem and FRH0201-Gem incubated with 10μM lapatinib (Lapa) (E, F) Relative mRNA levels and protein levels of ABCB1 in various CCA cell lines after treatment with gemcitabine (10 μM Gem) or a combination of gemcitabine and lapatinib (10μM Gem +5μM Lapa) for 48 h. (G) Upper left: The panoramic structure of ABCB1 and dFdCTP binding site. Upper right: A detailed three-dimensional plot of the interaction of dFdCTP and ABCB1. Bottom left: The panoramic structure of ABCB1 and lapatinib binding site. Bottom right: A detailed three-dimension plot of the interaction between lapatinib and ABCB1. The ABCB1 protein is depicted in red. H-bondings are shown in purple, hydrophobic bonds are shown in green, and mild polar bonds are shown in blue. Lapatinib and dFdCTP are depicted with the following color codes: carbon (blue), oxygen (red), nitrogen (dark blue), sulfur (yellow), fluoride (green), hydrogen (grey), chlorine (dark green), phosphorus (purple). (H) The luminescence increases in a dose-dependent manner following the incubation of verapamil (positive control), lapatinib or dFdCTP with P-glycoprotein-containing membranes. (I) ABCB1 ATPase activity increases in a dose-dependent manner with varying concentrations of verapamil, lapatinib, and dFdCTP. (J) The fluorescence intensity changes in rhodamine-dyed FRH0201-Gem after treatment with previously indicated concentrations of lapatinib. (K) Confocal images of CC6062 dyed with rhodamine after being treated with or without lapatinib. The data is expressed as the mean ± S.D., two-sided Student’s t-test, n.s. not significant, * p < 0.05, *** p < 0.001.

Article Snippet: The following primary antibodies were purchased from Cell Signaling Technology: phospho-Akt(4060), Akt(4691), phosphop-p44/42 MAPK(4370), p44/42 MAPK(4695), HER2(4290), phospho-HER2(2249), Cyclin D1(55506), p27 Kip1 (3686), c-myc(5605), ABCB1(13978), Na,K-ATPase α1 (23565, control for membrane proteins), and GAPDH(5174, control for total proteins).

Techniques: Expressing, Western Blot, Immunofluorescence, Fluorescence, Incubation, Binding Assay, Positive Control, Activity Assay