normal 16hbe cells  (BioVector NTCC)

Journal: Molecular Medicine Reports

Article Title: Identification and validation of biomarkers related to mitophagy in chronic obstructive pulmonary disease

doi: 10.3892/mmr.2025.13458

Figure Lengend Snippet: MTERF3 expression is upregulated in CSE-treated 16HBE cells and knockdown of its expression suppresses the induction of apoptosis of 16HBE cells exposed to CSE. (A) CCK-8 assay was used to detect 16HBE cell viability with or with CSE exposure. (B) Immunoblotting was employed to assess MTERF3 expression in 16HBE cells with or with CSE exposure. ***P<0.001 vs. control group. (C) Immunoblotting was used to assess MTERF3 expression in 16HBE cells following transfection. **P<0.01 and ***P<0.001 vs. siRNA-NC group. (D) The CCK-8 assay was used to detect the viability of MTERF3-silenced 16HBE cells exposed to CSE. (E) Flow cytometric analysis was used to detect the induction of apoptosis of MTERF3-silenced 16HBE cells exposed to CSE. (F) Immunoblotting was used to assess the expression of apoptosis-related proteins in MTERF3-silenced 16HBE cells exposed to CSE. ***P<0.001 vs. control group; # P<0.05, ## P<0.01 and ### P<0.001 vs. CSE + siRNA-NC group. MTERF3, mitochondrial transcription termination factor 3; CSE, cigarette smoke extract; CCK-8, Cell Counting Kit-8; cigarette smoke extract; siRNA, small interfering RNA; NC, negative control.

Article Snippet: The normal human bronchial epithelial cell line 16HBE was accessed from Procell Life Science & Technology Co., Ltd.

Techniques: Expressing, Knockdown, CCK-8 Assay, Western Blot, Control, Transfection, Cell Counting, Small Interfering RNA, Negative Control

Journal: Molecular Medicine Reports

Article Title: Identification and validation of biomarkers related to mitophagy in chronic obstructive pulmonary disease

doi: 10.3892/mmr.2025.13458

Figure Lengend Snippet: Knockdown of MTERF3 expression promotes mitophagy in CSE-treated 16HBE cells. (A) MDA content and (B) SOD activity were detected using the corresponding kits. (C) The generation of mitoROS was assessed with the application of Mito SOX Red staining. (D) MMP was evaluated using JC-1 staining. (E) Immunoblotting was employed to assess the expression of mitophagy-related proteins. ***P<0.001 vs. control group; # P<0.05, ## P<0.01 and ### P<0.001 vs. CSE + siRNA-NC group. MTERF3, mitochondrial transcription termination factor 3; CSE, cigarette smoke extract; MDA, malondialdehyde; SOD, superoxide dismutase; MMP, matrix metalloproteinase; JC-1, 5,5′,6,6′-tetrachloro1,1′,3,3′-tetramethylbenzimidazolylcarbocyanine iodide; siRNA, small interfering RNA; NC, negative control.

Article Snippet: The normal human bronchial epithelial cell line 16HBE was accessed from Procell Life Science & Technology Co., Ltd.

Techniques: Knockdown, Expressing, Activity Assay, Staining, Western Blot, Control, Small Interfering RNA, Negative Control

Journal: Thoracic Cancer

Article Title: Exosomal PVRL4 Promotes Lung Adenocarcinoma Progression by Enhancing the Generation of Myeloid‐Derived Suppressor Cell‐Secreted TGF ‐β1

doi: 10.1111/1759-7714.15495

Figure Lengend Snippet: PVRL4 silencing suppresses LUAD cell proliferation, invasion, and migration and induces cell apoptosis. (A‐G) The sh‐PVRL4 or sh‐NC was transfected into A549 and HCC827 cells. (A) Western blotting for PVRL4 levels in cells. (B‐D) CCK‐8 and colony formation assays for cell proliferation. (E) Transwell for cell invasion. (F) Wound healing assay for cell migration. (G) Flow cytometry analysis for cell apoptosis. * p < 0.05.

Article Snippet: LUAD cell lines A549 and HCC827 and the normal 16HBE cells were purchased from Procell (Wuhan, China) and then cultured in RPMI‐1640 medium (PM150110) plus1% penicillin/streptomycin (PB180120) and 10% FBS (164210‐50) (Procell) at 37°C with 5% CO 2 .

Techniques: Migration, Transfection, Western Blot, CCK-8 Assay, Wound Healing Assay, Flow Cytometry

Journal: Thoracic Cancer

Article Title: Exosomal PVRL4 Promotes Lung Adenocarcinoma Progression by Enhancing the Generation of Myeloid‐Derived Suppressor Cell‐Secreted TGF ‐β1

doi: 10.1111/1759-7714.15495

Figure Lengend Snippet: PVRL4 is transferred into PBMCs from LUAD cells by exosomes. (A) TEM analysis for exosome morphology. (B) Western blotting analysis for exosomal markers (CD9, CD63 and Alix). (C) The uptake of A549‐Exo and HCC827‐Exo was observed using the PKH67 staining. (D, E) Levels of PVRL4 protein were detected by western blotting in PMSCs after incubating with A549‐Exo, HCC827‐Exo or PBS (Control). (F, G) PBMCs were incubated with PBS, A549 or HCC827 cells and PBS, or A549 or HCC827 cells and GW4869, and levels of PVRL4 protein were examined by western blotting in PMSCs. * p < 0.05.

Article Snippet: LUAD cell lines A549 and HCC827 and the normal 16HBE cells were purchased from Procell (Wuhan, China) and then cultured in RPMI‐1640 medium (PM150110) plus1% penicillin/streptomycin (PB180120) and 10% FBS (164210‐50) (Procell) at 37°C with 5% CO 2 .

Techniques: Western Blot, Staining, Control, Incubation

Journal: Thoracic Cancer

Article Title: Exosomal PVRL4 Promotes Lung Adenocarcinoma Progression by Enhancing the Generation of Myeloid‐Derived Suppressor Cell‐Secreted TGF ‐β1

doi: 10.1111/1759-7714.15495

Figure Lengend Snippet: PVRL4 knockdown in LUAD cell exosomes suppresses MDSC induction and the level of MDSC‐secreted TGF‐β1. (A‐G) PBMCs were incubated with PBS, HCC827‐Exo sh–NC , A549‐Exo sh–NC , HCC827‐Exo sh–PVRL4 , or A549‐Exo sh–PVRL4 . (A) Levels of PVRL4 were detected by western blotting. (B, C) Flow cytometry for the number of CD14 + HLA‐DR − MDSCs after co‐incubation. (D‐G) ELISA analysis and western blotting for TGF‐β1 levels in PBMCs after co‐incubation. * p < 0.05.

Article Snippet: LUAD cell lines A549 and HCC827 and the normal 16HBE cells were purchased from Procell (Wuhan, China) and then cultured in RPMI‐1640 medium (PM150110) plus1% penicillin/streptomycin (PB180120) and 10% FBS (164210‐50) (Procell) at 37°C with 5% CO 2 .

Techniques: Knockdown, Incubation, Western Blot, Flow Cytometry, Enzyme-linked Immunosorbent Assay

Journal: Thoracic Cancer

Article Title: Exosomal PVRL4 Promotes Lung Adenocarcinoma Progression by Enhancing the Generation of Myeloid‐Derived Suppressor Cell‐Secreted TGF ‐β1

doi: 10.1111/1759-7714.15495

Figure Lengend Snippet: Knockdown of exosomal PVRL4 suppresses LUAD cell proliferation, invasion, and migration and induces cell apoptosis by regulating MDSC‐secreted TGF‐β1. (A‐K) A549 and HCC827 cells were incubated with TGF‐β1 overexpressed MDSCs, followed by incubating with HCC827‐Exo sh–NC , A549‐Exo sh–NC , HCC827‐Exo sh–PVRL4 , or A549‐Exo sh–PVRL4 . (A) Levels of PVRL4 were detected by western blotting. (B–E) CCK‐8 and colony formation assays for cell proliferation. (F, G) Transwell for cell invasion. (H, I) Wound healing assay for cell migration. (J, K) Flow cytometry analysis for cell apoptosis. * p < 0.05.

Article Snippet: LUAD cell lines A549 and HCC827 and the normal 16HBE cells were purchased from Procell (Wuhan, China) and then cultured in RPMI‐1640 medium (PM150110) plus1% penicillin/streptomycin (PB180120) and 10% FBS (164210‐50) (Procell) at 37°C with 5% CO 2 .

Techniques: Knockdown, Migration, Incubation, Western Blot, CCK-8 Assay, Wound Healing Assay, Flow Cytometry

Journal: Iranian Journal of Public Health

Article Title: CircABCB10 Promotes the Apoptosis and Inflammatory Response of 16HBE Cells by Cigarette Smoke Extract by Targeting miR-130a/PTEN Axis

doi: 10.18502/ijph.v53i3.15141

Figure Lengend Snippet: Expression levels of circABCB10, miR-130a and PTEN in 16HBE cells after CSE treatment Note: A,16HBE cells were treated with CSE at different concentrations (0%, 0.5%, 1%, 2%, 2% and 4%) for 48h, and circABCB10 expression at the mRNA level was determined by qRT-PCR; B, Detection of PTEN expression in cells; C, Detection of miR-130a expression in cells; D–F, Gene expression of circABCB10, miR-130a and PTEN in 16HBE cells treated with 4% CSE at different time, respectively. ** represents P <0.01

Article Snippet: The cells used in this study were 16HBE human normal bronchial epithelial cell line (purchased from ATCC, USA).

Techniques: Expressing, Quantitative RT-PCR, Gene Expression

Journal: Iranian Journal of Public Health

Article Title: CircABCB10 Promotes the Apoptosis and Inflammatory Response of 16HBE Cells by Cigarette Smoke Extract by Targeting miR-130a/PTEN Axis

doi: 10.18502/ijph.v53i3.15141

Figure Lengend Snippet: miR-130a inhibitor can reverse the biological effect of knocking down circABCB10 Note: A, The expression of miR-130a was determined by qRT-PCR; B, The proliferation of 16HBE cells was determined by CCK8; C-D, The expression level of apoptosis protein c-caspase 3 and the protein ratio of c-caspase 3/ t-caspase 3 were detected by Western blot; E–G, The changes of expression levels of cytokines, IL-1β, IL-6 and TNF-α in the supernatant were determined by ELISA. ** represents P <0.01

Article Snippet: The cells used in this study were 16HBE human normal bronchial epithelial cell line (purchased from ATCC, USA).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Iranian Journal of Public Health

Article Title: CircABCB10 Promotes the Apoptosis and Inflammatory Response of 16HBE Cells by Cigarette Smoke Extract by Targeting miR-130a/PTEN Axis

doi: 10.18502/ijph.v53i3.15141

Figure Lengend Snippet: circABCB10 was involved in the pathogenesis of COPD by regulating miR-130a/PTEN axis. Note: A, The mRNA level of PTEN were determined by qRT-PCR; B, The proliferation of 16HBE cells was determined by CCK8; C–D, The expression levels of the apoptotic protein c-caspase 3 and the protein ratio levels of ccaspase 3/T-caspase 3 were determined by Western blot; E–G, The changes of expression levels of cytokines, IL-1β, IL-6 and TNF-α in the supernatant of the medium were determined by ELISA. ** represents P <0.01

Article Snippet: The cells used in this study were 16HBE human normal bronchial epithelial cell line (purchased from ATCC, USA).

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Journal of Cell Communication and Signaling

Article Title: IncRNA AC004943.2 regulates miR‐135a‐5p and PTK2/P13K axis to promote laryngeal squamous cell carcinoma progression

doi: 10.1002/ccs3.12016

Figure Lengend Snippet: Knockdown of AC004943.2 inhibited LSCC progression. (A) RT‐qPCR was utilized to measure AC004943.2 in 16HBE and different LSCC cells. (B) Knockdown efficiency of AC004943.2 were examined through RT‐qPCR. (C) MTT was utilized to assess LSCC cell viability after AC004943.2 knockdown. (D) Colony formation was employed to evaluate the effects of AC004943.2 knockdown on LSCC proliferation. (E) Wound healing was utilized to analyze the effects of AC004943.2 knockdown on LSCC migration. (F) Transwell assay was applied to investigate LSCC invasion ability after inhibiting AC004943.2. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: Normal human bronchial epithelial cells 16HBE and LSCC cells TU686, AMC‐HN‐8, LSC‐1, TU177, and M4E were acquired from iCell Bioscience Inc (Shanghai, China).

Techniques: Knockdown, Quantitative RT-PCR, Migration, Transwell Assay