Journal: Oncology Letters

Article Title: LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches

doi: 10.3892/ol.2026.15671

Figure Lengend Snippet: Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in A549 (LUAD), SK-MES-1 (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.

Article Snippet: The A549 and SK-MES-1 cells (Procell Life Science & Technology Co., Ltd.) were divided into BC (blank control (BC), negative control (NC) and overexpression (OE) groups.

Techniques: Functional Assay, Expressing, Comparison, Western Blot, Biomarker Discovery, Over Expression, Transfection, Fluorescence, Labeling, MTT Assay, Flow Cytometry, Control, Negative Control, Infection, Real-time Polymerase Chain Reaction

Journal: Oncology Letters

Article Title: LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches

doi: 10.3892/ol.2026.15671

Figure Lengend Snippet: Influence of LATS2 overexpression on LUAD and LUSC cell migration and invasion. (A) Wound healing assay in A549 cells. (B) Wound healing assay in SK-MES-1 cell lines. (C) Transwell assay evaluating altered invasive capacity of A549 and SK-MES-1 cells. (D) Comparison of cell migration rates. (E) Comparison of number of invading cells. Scale bar, 100 µm, **P<0.01 and ***P<0.001. LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; LATS2, large tumor suppressor kinase 2; BC, blank control; NC, negative control; OE, overexpression.

Article Snippet: The A549 and SK-MES-1 cells (Procell Life Science & Technology Co., Ltd.) were divided into BC (blank control (BC), negative control (NC) and overexpression (OE) groups.

Techniques: Over Expression, Migration, Wound Healing Assay, Transwell Assay, Comparison, Control, Negative Control

Journal: Nature

Article Title: In vivo site-specific engineering to reprogram T cells

doi: 10.1038/s41586-026-10235-x

Figure Lengend Snippet: a , Tumour challenge schematic for multiple myeloma. NSG MHC-I/II double-KO mice received i.v. OPM2 cells (1 × 10 6 ), followed 5 days later by human PBMCs (1 × 10 7 ). Then, 5 days after PBMC transfer, mice received PBS or anti-CD3-EDV (5 × 10 11 sgRNAs per mouse; Cas9–sgTRAC) plus AAV-hT7 (1 × 10 12 vg per mouse), delivering a TRAC HDRT encoding a BCMA-1XX-CAR-P2A-EGFRt. The tumour burden was monitored using BLI. At day 35 after EDV/AAV treatment, mice were rechallenged i.v. with OPM2 cells (5 × 10 6 ). b , BLI measurements in mice injected with OPM2 alone ( n = 5), OPM2 + PBMC ( n = 8) or OPM2 + PBMC + EDV/AAV ( n = 8). Rechallenge was performed in four EDV/AAV-treated mice that controlled tumour growth by day 35 and in five age-matched control mice. BLI values represent the mean of dorsal and ventral signals (photons per s per cm 2 ). c , Tumour challenge schematic for solid tumours. NSG MHC-I/II double-KO mice received subcutaneous (s.c.) MES-SA cells (4 × 10 6 ), followed 4 days later by human PBMCs (1 × 10 7 ). Then, 3 days after PBMC transfer, mice received PBS or anti-CD3-EDV (5 × 10 11 sgRNAs per mouse) plus AAV-hT7 (1 × 10 12 vg per mouse), delivering a TRAC HDRT encoding an anti-B7H3-CD28ζ-1XX-CAR-P2A-EGFRt. The tumour burden was assessed by calliper measurements. d , Kaplan–Meier survival analysis of mice bearing MES-SA tumours; MES-SA only ( n = 4), MES-SA + PBMC ( n = 5) or MES-SA + PBMC + EDV/AAV (anti-B7H3–CD28ζ−1XX TRAC CAR; n = 6). e , Tumour growth measurements from the mice in d . CR, complete response. Images in a and c were adapted from Servier Medical Art ( https://smart.servier.com/ ), under a CC BY 4.0 licence.

Article Snippet: MES-SA cells (ATCC, CRL-1976) were cultured in McCoy’s 5a modified medium (Gibco, 16600082) supplemented with 10% FBS and penicillin–streptomycin.

Techniques: Injection, Control

Journal: Nature

Article Title: In vivo site-specific engineering to reprogram T cells

doi: 10.1038/s41586-026-10235-x

Figure Lengend Snippet: a , Dorsal images from mice described in Fig. . BLI is displayed as radiance (p/sec/cm 2 /sr). Days are indicated from time of PBS or EDV/AAV treatment. Day 11, 14, 21, 28 ans 35 are shown with and without mice that are saturating the signal. b , Total body weight from mice in Fig. . c , Experimental conditions from Fig. were repeated with an additional PBMC donor. Kaplan-Meier survival analysis in mice injected with MES-SA only (n = 4), MES-SA and PBMC (n = 5), MES-SA, PBMC and EDV/AAV targeting a aB7H3-CD28z-1XX (n = 6) CAR to TRAC . d , Tumour measurements in mice injected with MES-SA only (n = 4), MES-SA and PBMC (n = 5), MES-SA, PBMC and EDV/AAV targeting a aB7H3-CD28z-1XX (n = 8) CAR to TRAC . e , Total body weight from mice in c , d .

Article Snippet: MES-SA cells (ATCC, CRL-1976) were cultured in McCoy’s 5a modified medium (Gibco, 16600082) supplemented with 10% FBS and penicillin–streptomycin.

Techniques: Injection