Journal: Advances in Radiation Oncology

Article Title: Synergistic Effect of Linebacker-1 With Radiation Therapy in a Mouse Lung Cancer Model

doi: 10.1016/j.adro.2026.102051

Figure Lengend Snippet: Biochemical structures of Linebacker-1 (LB1) and myricetin and antineoplastic effect of LB1 with/without radiation in human colon and lung cell lines. (A) Myricetin (left) and LB1 (right) showing with a red circle for the OH ion’s replacement by a cloride ion (Cl). (B) Schematic diagram of the treatment design using LB1 for in vitro study. (C) and (D) MTT growth assay using OD value 570 nm, showing the antitumor effect of LB1 in titrated doses for both human colon (HT29) and lung (A549) cancer cell lines, respectively. (E) Bar graph representing the colony count numbers from the clonogenic survival assay after LB1 treatment. (F) Schematic diagram showing the treatment design for in vitro LB1 and radiation treatment. Doses of 0, 25, 50, and 75 µM LB1, along with single radiation fractions of 0, 2, 4, and 6 Gy, were used in the clonogenic survival study. (G) For the clonogenic survival assay, colony counts are shown for A549 cells treated with 0, 2, 4, and 6 Gy of radiation, with or without LB1, at 0, 25, 50, and 75 µM. (H) colony count for A549 and Lewis lung carcinoma (LLC1) cell line , respectively. Graphs are generated from the average of at least 3 study repeats. The SD of the multiple independent repeats is shown, while statistical significance is shown by *** P < .001. Abbreviation : OD = optical density; OH = hydroxide ion; MTT = methyl dimethylthiazol diphenyltetrazolium bromide; RT = radiation therapy.

Article Snippet: A549 cells were cultured in RPMI cell culture media (Gibco), the HT29 cell line was cultured in McCoy’s 5A medium (ATCC), and the LLC1 cell was cultured in Dulbecco’s Modified Eagle Media (Gibco).

Techniques: In Vitro, Growth Assay, Clonogenic Cell Survival Assay, Generated

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: oHSV-1 exhibits the characteristics of a standard one-step growth curve and can efficiently replicate and express exogenous genes (A) The results of virus titer determination of HSV-1/WT, RG2001m, RG2002m, RG2005m, RG2011m, and RG2012m in Vero cells 48 h after infection. (B) Vero cells were infected with oHSV-1 at a multiplicity of infection (MOI) = 1, and the virus titers were determined at 0, 8, 16, 24, 32, 40, and 48 h, respectively, and a growth curve was drawn. (C) The results of virus titer determination of oHSV-1 in colon cancer cells (CT26, HCT116, and HT29) 48 h after infection. (D–F) The growth curves of oHSV-1 in colon cancer cells (CT26, HCT116, and HT29). (G) At MOI = 10, IL-15 expression levels in cell supernatants of HSV-1/WT, RG2001m, RG2005m, and RG2012m at 24, 48, and 72 h post-infection (mouse IL-15 ELISA Kit, elabscience). (H) At MOI = 10, IL-12 expression levels in cell supernatants of HSV-1/WT, RG2002m, RG2005m, and RG2012m at 24, 48, and 72 h post-infection (mouse IL-12 ELISA Kit, elabscience). (I) At MOI = 10, chemokine CCL5 expression levels in cell supernatants of HSV-1/WT, RG2011m, and RG2012m at 24, 48, and 72 h post-infection (mouse CCL5 ELISA Kit, elabscience). (Data are presented as mean ± SD. Comparisons between datasets were performed using one-way ANOVA and Student’s t test, with p values calculated [ n = 3]) ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗).

Article Snippet: CT26, HTC116, and HT29 cells were purchased from Wuhan Procell Life Science & Technology Co., Ltd., China (Cat. No. CL-0071; Cat. No. CL-0096; Cat. No. CL-0118).

Techniques: Virus, Infection, Expressing, Enzyme-linked Immunosorbent Assay

Journal: iScience

Article Title: Triple-armed oncolytic HSV enhances antitumor immunity by remodeling the tumor microenvironment in subcutaneous murine CRC

doi: 10.1016/j.isci.2026.115883

Figure Lengend Snippet: Killing effect of recombinant oHSV-1 on colon cancer cells (A–C) CT26 (A), HCT116 (B), and HT29 (C) colon cancer cells were infected with recombinant oncolytic virus at multiplicity of infection (MOI) of 0.5, 1, and 5, respectively. The cell killing rate was detected by cell counting kit-8 (CCK8) assay 48 h after infection. The results showed that the killing effect of the virus on the three colon cancer cells was enhanced in an MOI - dependent manner. (D–F) CT26 (D), HCT116 (E), and HT29 (F) cells were infected with recombinant oncolytic virus at MOI = 1. The killing rate was measured by CCK8 assay at 24, 48, and 72 h after infection, suggesting that the killing effect of the virus on colon cancer cells was significantly enhanced with the prolongation of action time. (The values are presented as mean ± SD. The datasets were compared via one-way ANOVA. n = 3) ( p > 0.05, ns; p < 0.05, ∗; p < 0.01, ∗ ∗; p < 0.001, ∗ ∗ ∗.).

Article Snippet: CT26, HTC116, and HT29 cells were purchased from Wuhan Procell Life Science & Technology Co., Ltd., China (Cat. No. CL-0071; Cat. No. CL-0096; Cat. No. CL-0118).

Techniques: Recombinant, Infection, Virus, Cell Counting, CCK-8 Assay

Journal: Human Mutation

Article Title: PLSCR3 Deficiency Triggers mtDNA‐Driven cGAS‐STING Activation to Potentiate Antitumor Immunity in Colorectal Cancer

doi: 10.1155/humu/8545428

Figure Lengend Snippet: PLSCR3 deficiency disrupts mitochondrial homeostasis in CRC cells. (A) Western blotting verified the reduction of PLSCR3 protein levels in HT29 cells. (B) RT‐qPCR analysis verified reduction of PLSCR3 mRNA levels normalized to GAPDH compared with negative control (NC) cells ( p < 0.0001, n = 3). (C) Representative JC‐1 staining (scale bar: 20 μ m) images showing red fluorescence (polarized mitochondria) and green fluorescence (depolarized mitochondria). (D) Quantification of the JC‐1 red/green fluorescence intensity ratio. Fluorescence intensity was quantified using ImageJ software as described in the section. (E) Real‐time oxygen consumption rate (OCR) profiles under sequential treatment with oligomycin, FCCP, and rotenone/Antimycin A. (F) Quantification of cytosolic mtDNA by qPCR using the D‐loop ratio in PLSCR3‐knockdown and control cells. Data are presented as mean ± SD from three independent experiments. Statistical significance was determined using an unpaired two‐tailed Student′s t ‐test for two‐group comparisons.

Article Snippet: The human colon carcinoma cell line HT29 (Cat. No. ATCC‐HTB‐38) and the mouse colon carcinoma cell line CT26.WT (Cat. No. CRL‐2638, ATCC, Virginia, United States) were maintained in RPMI 1640 medium (Cat. No. BC‐M‐017, Bio‐Channel, Jiangsu, China) supplemented with 10% fetal bovine serum.

Techniques: Western Blot, Quantitative RT-PCR, Negative Control, Staining, Fluorescence, Software, Knockdown, Control, Two Tailed Test

Journal: Human Mutation

Article Title: PLSCR3 Deficiency Triggers mtDNA‐Driven cGAS‐STING Activation to Potentiate Antitumor Immunity in Colorectal Cancer

doi: 10.1155/humu/8545428

Figure Lengend Snippet: PLSCR3 deficiency activates mtDNA‐associated cGAS‐STING signaling. (A) 2 ′ ‐3 ′ ‐cGAMP quantification by ELISA in PLSCR3 knockdown (KD_PLSCR3) HT29 cells and normal controls (NCs) treated with Scramble or dideoxycytidine (DDC) ( p < 0.0001; ns = not significant; n = 3). (B, C) KD_PLSCR3 cells exhibited an elevation in IFN β and CXCL10 production measured by ELISA compared to NC ( p < 0.0001, n = 3). CRISPR‐mediated STING knockout (STING sg) completely abrogated these effects. (D) Western blot analysis showed upregulation of phosphorylated STING and innate immune effectors (IFIH1, ISG60, and ISG15 protein) in STING‐competent KD_PLSCR3 cells relative to GAPDH loading controls. (E) Normalized mRNA level quantification by qPCR demonstrated significant induction of interferon‐stimulated genes (ISGs) in STING‐competent KD_PLSCR3 cells compared with the other groups. Data in panels A–C and E are presented as mean ± SD. Statistical significance was determined using one‐way ANOVA followed by Tukey′s multiple‐comparisons post hoc test for multiple‐group comparisons.

Article Snippet: The human colon carcinoma cell line HT29 (Cat. No. ATCC‐HTB‐38) and the mouse colon carcinoma cell line CT26.WT (Cat. No. CRL‐2638, ATCC, Virginia, United States) were maintained in RPMI 1640 medium (Cat. No. BC‐M‐017, Bio‐Channel, Jiangsu, China) supplemented with 10% fetal bovine serum.

Techniques: Enzyme-linked Immunosorbent Assay, Knockdown, CRISPR, Knock-Out, Western Blot

Journal: Human Mutation

Article Title: PLSCR3 Deficiency Triggers mtDNA‐Driven cGAS‐STING Activation to Potentiate Antitumor Immunity in Colorectal Cancer

doi: 10.1155/humu/8545428

Figure Lengend Snippet: PLSCR3 deficiency enhances the sensitivity to immune cell–mediated killing in CRC. (A) Schematic of coculture system: PLSCR3 knockdown (KD_PLSCR3) HT29 cells or control were cocultured with human cord blood–derived NK cells at an E:T ratio of 5:1. (B, C) Phase‐contrast microscopy (scale bar: 50 μ m) showing morphological changes. Morphological analysis demonstrated decreased cell number in KD_PLSCR3 cells in the coculture condition ( p < 0.0001, n = 5). (D) Mouse graft carcinoma with control or PLSCR3 knockout (PLSCR3 sg) CT26 cells were treated with or without anti‐PD‐1 antibodies ( α PD‐1). Tumor growth curves (mm 3 ) were recorded at Days 5, 10, 15, and 20 after tumor cell inoculation in immunocompetent BALB/c mice. (E) At Day 20, terminal tumor weights in the mouse graft carcinoma were measured. (F–H) Flow cytometry analysis of CD4+ and CD8+ tumor‐infiltrating T cells. The representative cell populations of CD4+ and CD8+ are shown. (I, J) Flow cytometry and ELISA analysis of Granzyme B (GZMB) expression ( n = 5). Data are presented as mean ± SD. Tumor growth curves were analyzed using two‐way repeated‐measures ANOVA with post hoc multiple‐comparison tests. For multiple‐group comparisons, including panels I and J, one‐way ANOVA followed by Tukey′s post hoc test was used.

Article Snippet: The human colon carcinoma cell line HT29 (Cat. No. ATCC‐HTB‐38) and the mouse colon carcinoma cell line CT26.WT (Cat. No. CRL‐2638, ATCC, Virginia, United States) were maintained in RPMI 1640 medium (Cat. No. BC‐M‐017, Bio‐Channel, Jiangsu, China) supplemented with 10% fetal bovine serum.

Techniques: Knockdown, Control, Derivative Assay, Microscopy, Knock-Out, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Expressing, Comparison