Journal: Nanomedicine : nanotechnology, biology, and medicine

Article Title: Imaging the Delivery of Drug-loaded, Iron-stabilized Micelles

doi: 10.1016/j.nano.2017.01.009

Figure Lengend Snippet: Efficacy results in colorectal (HT-29, HCT116) and lung (NCI-H460, A549) models treated with IT-141 or IT-147.

Article Snippet: Cell Culture HCT116 colorectal carcinoma (no. CCL-247), HT1080 fibrosarcoma (no. CCL-121), HT-29 colorectal adenocarcinoma (no. HTB-38), MCF-7 breast adenocarcinoma (no. HTB-22), and A549 (no. CCL-185) and NCI-H460 (no. HTB-177) lung carcinomas were all purchased from ATCC (Manassas, VA, USA) and maintained in appropriate growth media.

Techniques: Formulation, Control

Journal: Thoracic Cancer

Article Title: microRNA ‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting HOXA1

doi: 10.1111/1759-7714.13459

Figure Lengend Snippet: miR‐100 inhibited NSCLC cell proliferation. ( a ) qRT‐PCR was used to measure miR‐100 expressions in NSCLC cells. ( b , c ) miR‐100 overexpression or inhibition was confirmed by qRT‐PCR. ( d , e ) MTT assays were performed to detect the functions of miR‐100 in NSCLC cell proliferation. * P < 0.05, ** P < 0.01, *** P < 0.001 (d: NC and miR‐100 mimics; e: NC and miR‐100 inhibitor).

Article Snippet: Human normal bronchial epithelium cell BEAS‐2B and NSCLC cells (NCI‐H460, NCI‐H1299, SPC‐A1 and A549) were purchased from ATCC and maintained in DMEM (Gibco; Thermo Fisher Scientifc, Inc., Waltham, MA, USA) which contained 10% FBS (Gibco; Thermo Fisher Scientifc, Inc.) in a humidified atmosphere with 5% CO 2 at 37°C.

Techniques: Quantitative RT-PCR, Over Expression, Inhibition

Journal: Thoracic Cancer

Article Title: microRNA ‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting HOXA1

doi: 10.1111/1759-7714.13459

Figure Lengend Snippet: miR‐100 suppressed the cell invasion and migration abilities of NSCLC cells. ( a , b ) The impacts of miR‐100 restoration on NSCLC cell invasion and migration were determined using transwell assays. ( c , d ) Transwell assay was performed to determine invasion and migration capacities of miR‐100 suppressed NSCLC cells. ** P < 0.01, *** P < 0.001.

Article Snippet: Human normal bronchial epithelium cell BEAS‐2B and NSCLC cells (NCI‐H460, NCI‐H1299, SPC‐A1 and A549) were purchased from ATCC and maintained in DMEM (Gibco; Thermo Fisher Scientifc, Inc., Waltham, MA, USA) which contained 10% FBS (Gibco; Thermo Fisher Scientifc, Inc.) in a humidified atmosphere with 5% CO 2 at 37°C.

Techniques: Migration, Transwell Assay

Journal: Thoracic Cancer

Article Title: microRNA ‐100 functions as a tumor suppressor in non‐small cell lung cancer via regulating epithelial‐mesenchymal transition and Wnt/β‐catenin by targeting HOXA1

doi: 10.1111/1759-7714.13459

Figure Lengend Snippet: HOXA1 was a direct target of miR‐100 in NSCLC cells. ( a )The WT and MUT binding sites of miR‐100 on HOXA1 3′‐UTR. ( b ) Dual‐luciferase reporter assay was used to confirm the association between miR‐100 and HOXA1 in NSCLC cells ( NC and miR‐100 mimics). ( c , d ) Regulatory effects of miR‐100 on HOXA1 expressions in NSCLC cells. * P < 0.05, ** P < 0.01.

Article Snippet: Human normal bronchial epithelium cell BEAS‐2B and NSCLC cells (NCI‐H460, NCI‐H1299, SPC‐A1 and A549) were purchased from ATCC and maintained in DMEM (Gibco; Thermo Fisher Scientifc, Inc., Waltham, MA, USA) which contained 10% FBS (Gibco; Thermo Fisher Scientifc, Inc.) in a humidified atmosphere with 5% CO 2 at 37°C.

Techniques: Binding Assay, Luciferase, Reporter Assay

Journal: Molecular and Cellular Biology

Article Title: Breast Cancer Metastasis Suppressor 1 Functions as a Corepressor by Enhancing Histone Deacetylase 1-Mediated Deacetylation of RelA/p65 and Promoting Apoptosis

doi: 10.1128/mcb.00940-06

Figure Lengend Snippet: FIG. 1. BRMS1 expression is reduced in NSCLC cells and tumor tissues. (A) BRMS1 mRNA and protein expression in tumorigenic but nonmetastatic cell lines (NL20 and HEK 293T) and NSCLC cell lines (H358, H1299, H157, A549, and H460). mRNA levels were evaluated by quantitative RT-PCR and calculated as a ratio to the human pla- centa control (top). Protein levels of BRMS1 were detected by West- ern blotting with -tubulin as a loading control (bottom). Real-time RT-PCR data represent the mean the SD of three experiments performed in triplicate. (B) BRMS1 mRNA and protein expression in tumor tissues and patient-matched adjacent lung tissues. mRNA and protein levels for patient-matched samples were determined as in panel A. The pathological stage is presented using the international staging system for lung cancer (44). Stage IA NSCLC has limited local disease with no metastasis to lymph nodes. Stage IIB NSCLC includes spread to local lymph nodes. Stage IIIB disease includes metastasis to regional lymph nodes outside of the lung itself.

Article Snippet: Human NSCLC lines (NCI-H157, NCI-H358, NCI-H460, NCI-A549, and NCI-H1299), a normal human bronchial epithelial cell line (NL-20), and tumorigenic but nonmetastatic human embryonic kidney cells (HEK 293T) (63) were obtained from the American Type Culture Collection (Manassas, VA).

Techniques: Expressing, Quantitative RT-PCR, Control

Journal: Molecular and Cellular Biology

Article Title: Breast Cancer Metastasis Suppressor 1 Functions as a Corepressor by Enhancing Histone Deacetylase 1-Mediated Deacetylation of RelA/p65 and Promoting Apoptosis

doi: 10.1128/mcb.00940-06

Figure Lengend Snippet: FIG. 7. BRMS1 sensitizes NSCLC cells to apoptosis. (A) 293T cells and H1299 cells were transiently transfected with expression vector encoding BRMS1 or empty vector control. At 24 h after transfection, cells were treated or not treated with TNF (50 ng/ml) for an additional 24 h. Cell extracts were analyzed for DNA fragmentation as a marker for apoptosis. and , P 0.05 and P 0.01, respectively, compared to CMV plus No Add groups; # and ##, P 0.05 P 0.01, respectively, compared to CMV plus TNF groups. (B) 293T cells and H1299 cells were transfected and treated as described above. Cell extracts were analyzed for caspase-3 activation as a marker for apoptosis. (C) 293T and H1299 cells were transfected with pCMV-BRMS1 versus pCMV empty vector (Control) or with siRNA-BRMS1 versus siRNA-control as indicated. At 48 h after transfection, cells were suspended for various lengths of time. Cell death was measured by trypan blue exclusion assays. Western blots show that siRNA specifically knocks down BRMS1 protein expression. and , P 0.05 and P 0.01, respectively, compared to CMV or siRNA control at each time point; #, P 0.05 compared to time zero groups.

Article Snippet: Human NSCLC lines (NCI-H157, NCI-H358, NCI-H460, NCI-A549, and NCI-H1299), a normal human bronchial epithelial cell line (NL-20), and tumorigenic but nonmetastatic human embryonic kidney cells (HEK 293T) (63) were obtained from the American Type Culture Collection (Manassas, VA).

Techniques: Transfection, Expressing, Plasmid Preparation, Control, Marker, Activation Assay, Western Blot