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ATCC murine colon cancer cell line ct26 cl25
Murine Colon Cancer Cell Line Ct26 Cl25, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 162 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ct26+murine+colon+cancer/CT26%2ECL25/pmc13149252-33-1-19
Average 95 stars, based on 162 article reviews

murine colon cancer cell line ct26 cl25 - by Bioz Stars, 2026-09

95/100 stars

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Article Title: Intratumoral injection of inactivated Sendai virus particles elicits strong antitumor activity by enhancing local CXCL10 expression and systemic NK cell activation
Article Snippet: Renca renal cell carcinoma (RCC) was purchased from the American Type Culture Collection (Manassas, VA) and was cultured in RPMI 1640 medium (Nakarai Tesque, Kyoto, Japan) with 10% fetal bovine serum (FBS) (Bio West, Miami, FL) and antibiotics (100 U/ml penicillin and 100 μg/ml streptomycin, Nakarai Tesque, Kyoto, Japan). .. CT26 murine colon cancer and B16 melanoma were purchased from the American Type Culture Collection and cultured in DMEM (Nakarai Tesque, Kyoto, Japan) with 10% FBS and antibiotics (100 U/ml penicillin and 100 μg/ml streptomycin). ..

Article Title: Preparation and Characterization of Gelonin-Melittin Fusion Biotoxin for Synergistically Enhanced Anti-Tumor Activity
Article Snippet: .. Cell Culture HeLa human cervical cancer, 9L rat glioma, U87 MG human glioblastoma-astrocytoma, CT26 murine colon cancer, LS174T human adenocarcinoma and MDCK (Madin-Darby canine kidney) cells were purchased from American Type Culture Collection (ATCC, Manassas, VA). ..

Article Title: Intratumoral injection of inactivated Sendai virus particles elicits strong antitumor activity by enhancing local CXCL10 expression and systemic NK cell activation.
Article Snippet: We have already demonstrated that inactivated, replication-defective Sendai virus particles (HVJ-E) have a powerful antitumor eVect by both the generation of tumorspeciWc cytotoxic T cells and inhibition of regulatory T cell activity.. Here, we report that HVJ-E also has an antitumor eVect through non-T cell immunity.. Microarray analysis revealed that direct injection of HVJ-E induced the expression of CXCL10 in established Renca tumors.

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Comparison of systemic delivery of FusOn-CD47-luc and FusOn-luc in immune-competent mice pre-immunized with HSV-2 (A) Schematic illustration of the FusOn-series viruses used in this study. The parental FusOn-H2 was generated by replacing the N-terminal domain of the ICP10 gene, which encodes the large subunit of ribonucleotide reductase (RR), with GFP. The locations of glycoprotein C (gC), the terminal repeat long (TR L ) and short (TR S ) regions, and the internal repeats (IR) are indicated. FusOn-luc was constructed by inserting a luciferase gene cassette ( luc ) upstream of the gC locus, whereas FusOn-CD47-luc was generated by fusing the extracellular domain (ECD) of CD47 to gC and inserting the luc cassette at the same position. (B) IVIS imaging of virus distribution following systemic delivery. Balb/c mice were first immunized twice with a gH-deleted infectious single-cycle HSV-2 (DISC-HSV2) before implantation with CT26 tumor cells in the right flank. Once tumors reached approximately 8 mm in diameter, mice received one of the three viruses via tail vein injection at a dose of 2 × 10 6 PFU. Bioluminescence imaging was performed using an IVIS imager on the indicated days post-injection. The locations of the liver and tumor are indicated by red arrows. Representative images from one of five mice in each treatment group are shown.

Journal: Molecular Therapy Oncology

Article Title: Strategically engineering an oncolytic herpes simplex virus to improve systemic delivery

doi: 10.1016/j.omton.2026.201132

Figure Lengend Snippet: Comparison of systemic delivery of FusOn-CD47-luc and FusOn-luc in immune-competent mice pre-immunized with HSV-2 (A) Schematic illustration of the FusOn-series viruses used in this study. The parental FusOn-H2 was generated by replacing the N-terminal domain of the ICP10 gene, which encodes the large subunit of ribonucleotide reductase (RR), with GFP. The locations of glycoprotein C (gC), the terminal repeat long (TR L ) and short (TR S ) regions, and the internal repeats (IR) are indicated. FusOn-luc was constructed by inserting a luciferase gene cassette ( luc ) upstream of the gC locus, whereas FusOn-CD47-luc was generated by fusing the extracellular domain (ECD) of CD47 to gC and inserting the luc cassette at the same position. (B) IVIS imaging of virus distribution following systemic delivery. Balb/c mice were first immunized twice with a gH-deleted infectious single-cycle HSV-2 (DISC-HSV2) before implantation with CT26 tumor cells in the right flank. Once tumors reached approximately 8 mm in diameter, mice received one of the three viruses via tail vein injection at a dose of 2 × 10 6 PFU. Bioluminescence imaging was performed using an IVIS imager on the indicated days post-injection. The locations of the liver and tumor are indicated by red arrows. Representative images from one of five mice in each treatment group are shown.

Article Snippet: African green monkey kidney (Vero) cells, CT26 murine colon cancer cells, LL/2 murine lung cancer cells, and HCT116 human colorectal cancer cells were purchased from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Comparison, Generated, Construct, Luciferase, Imaging, Virus, Injection

Tumor delivery efficiency of FusOn-SD following systemic delivery in vivo (A) Sequential images of one representative mouse from each group (five mice per group) at the indicated time points after systemic administration of FusOn-SD in immune-competent, CT26-tumor-bearing Balb/c mice pre-immunized with HSV-2. The experimental procedure was identical to that in B. (B) Effect of adoptively transferred human anti-HSV-2 sera on the systemic delivery of FusOn-SD to xenografted human tumors. Mpanc-96 human pancreatic cancer cells were implanted in the right flank of immunodeficient mice. Once tumors reached an approximate size of 8 mm in diameter, mice received an adoptive transfer of 100 μL of either a mixture of eight human anti-HSV-2 sera or non-immune sera as a control, followed by tail vein injection of 2 × 10 6 PFU FusOn-SD. Shown are IVIS images taken 48 h after virus administration, with the tumor sites and corresponding bioluminescent signals highlighted by red circles.

Journal: Molecular Therapy Oncology

Article Title: Strategically engineering an oncolytic herpes simplex virus to improve systemic delivery

doi: 10.1016/j.omton.2026.201132

Figure Lengend Snippet: Tumor delivery efficiency of FusOn-SD following systemic delivery in vivo (A) Sequential images of one representative mouse from each group (five mice per group) at the indicated time points after systemic administration of FusOn-SD in immune-competent, CT26-tumor-bearing Balb/c mice pre-immunized with HSV-2. The experimental procedure was identical to that in B. (B) Effect of adoptively transferred human anti-HSV-2 sera on the systemic delivery of FusOn-SD to xenografted human tumors. Mpanc-96 human pancreatic cancer cells were implanted in the right flank of immunodeficient mice. Once tumors reached an approximate size of 8 mm in diameter, mice received an adoptive transfer of 100 μL of either a mixture of eight human anti-HSV-2 sera or non-immune sera as a control, followed by tail vein injection of 2 × 10 6 PFU FusOn-SD. Shown are IVIS images taken 48 h after virus administration, with the tumor sites and corresponding bioluminescent signals highlighted by red circles.

Techniques: In Vivo, Adoptive Transfer Assay, Control, Injection, Virus

In vivo evaluation of the antitumor effect of FusOn-SD in immune syngeneic tumor models in immune-competent animals (A) Evaluation of FusOn-SD in the murine CT26 colon cancer model. Immune-competent Balb/c mice were immunized with HSV-2 before CT26 cells were implanted subcutaneously. Oncolytic viruses were given intratumorally at a dose of 2 × 10 6 PFU. Tumor size was measured at the indicated time points and plotted. ★ p < 0.05 compared with other oncolytic viruses and PBS; p < 0.05 compared with PBS. (B) Evaluation of FusOn-SD in the murine LL/2 lung cancer model. Immune-competent C57BL6 mice were immunized with HSV-2 before LL/2 cells were implanted subcutaneously. When tumor became palpable, 2 × 10 6 PFU of the indicated oncolytic viruses were given via the tail vein, either alone or in combination with CP and/or PD1 mAb (detailed treatment schemes are provided in the section). Tumor size was measured at the indicated time points and plotted. Due to the rapid growth of these two tumor models in the control group, the experiments were terminated early to address ethical concerns for animal welfare. ★ p < 0.05 compared with other treatment groups and PBS; p < 0.05 compared with PBS.

Journal: Molecular Therapy Oncology

Article Title: Strategically engineering an oncolytic herpes simplex virus to improve systemic delivery

doi: 10.1016/j.omton.2026.201132

Figure Lengend Snippet: In vivo evaluation of the antitumor effect of FusOn-SD in immune syngeneic tumor models in immune-competent animals (A) Evaluation of FusOn-SD in the murine CT26 colon cancer model. Immune-competent Balb/c mice were immunized with HSV-2 before CT26 cells were implanted subcutaneously. Oncolytic viruses were given intratumorally at a dose of 2 × 10 6 PFU. Tumor size was measured at the indicated time points and plotted. ★ p < 0.05 compared with other oncolytic viruses and PBS; p < 0.05 compared with PBS. (B) Evaluation of FusOn-SD in the murine LL/2 lung cancer model. Immune-competent C57BL6 mice were immunized with HSV-2 before LL/2 cells were implanted subcutaneously. When tumor became palpable, 2 × 10 6 PFU of the indicated oncolytic viruses were given via the tail vein, either alone or in combination with CP and/or PD1 mAb (detailed treatment schemes are provided in the section). Tumor size was measured at the indicated time points and plotted. Due to the rapid growth of these two tumor models in the control group, the experiments were terminated early to address ethical concerns for animal welfare. ★ p < 0.05 compared with other treatment groups and PBS; p < 0.05 compared with PBS.

Techniques: In Vivo, Control

A Western blot analysis of the Smad2/3 expressions in wide-type-derived CD11b + Gr-1 + cells (WT) and CT26-derived spleen CD11b + Gr-1 + MDSC (Tu). B Quantification of relative Smad3 transcription levels in wide-type-derived CD11b + Gr-1 + cells (WT) and CT26-derived spleen CD11b + Gr-1 + MDSC (Tu). C FCM analysis of the Smad3 expressions in HLA-DR − CD33 + CD11b + MDSC derived from peripheral blood of CRC patients ( n = 30) and healthy donors ( n = 29). D Western blot analysis of the Smad3 expressions in wide-type-derived CD11b + Gr-1 + cells (WT) and MDSC with tumor progression of CT26 mouse models respectively at early (8 d), middle (18 d), and late stage (28 d). E FCM analysis of the proportions of CD11b + Ly6C hi , CD11b + Ly6C mid , and CD11b + Ly6C lo cells in the EGFP + CD11b + cells of bone marrow from AAV9-Smad3/vector group of mice. F FCM analysis of the proportions of CD11b + Ly6G hi cells in the EGFP + CD11b + cells of bone marrow from AAV9-Smad3/vector group of mice. G FCM analysis of the expressions of CD86 in the EGFP + CD11b + cells of bone marrow from AAV9-Smad3/vector group of mice. H Cell numbers in control group, 2 μM SIS3 treatment group, 20 ng/mL Tgfβ1 treatment group and Tgfβ1 + SIS3 treatment group after MΦ induction by 20 ng/mL M-CSF for 7 days and DC induction by 20 ng/mL GM-CSF and 10 ng/mL IL-4 for 9 days. I – K Analyzing DC and MΦ proportions, MHCII and Ki67 expressions, and cellular morphology of each treatment group respectively in DC and MΦ induction system. L Western blot analysis of the Smad3 expressions in initial bone marrow cells (BMC) and BMC-induced MΦ, DC, and MO-MDSC. Except C ( n = 29), error bars of statistical graphs represent mean ± SD, n = 3. For ( A – C , E – G ), p -values were determined using two sides unpaired t-test; For ( D , H – J ), p -values were determined using one-way ANOVA with Tukey test. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns no significant.

Journal: Cell Death & Disease

Article Title: Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer

doi: 10.1038/s41419-025-08228-1

Figure Lengend Snippet: A Western blot analysis of the Smad2/3 expressions in wide-type-derived CD11b + Gr-1 + cells (WT) and CT26-derived spleen CD11b + Gr-1 + MDSC (Tu). B Quantification of relative Smad3 transcription levels in wide-type-derived CD11b + Gr-1 + cells (WT) and CT26-derived spleen CD11b + Gr-1 + MDSC (Tu). C FCM analysis of the Smad3 expressions in HLA-DR − CD33 + CD11b + MDSC derived from peripheral blood of CRC patients ( n = 30) and healthy donors ( n = 29). D Western blot analysis of the Smad3 expressions in wide-type-derived CD11b + Gr-1 + cells (WT) and MDSC with tumor progression of CT26 mouse models respectively at early (8 d), middle (18 d), and late stage (28 d). E FCM analysis of the proportions of CD11b + Ly6C hi , CD11b + Ly6C mid , and CD11b + Ly6C lo cells in the EGFP + CD11b + cells of bone marrow from AAV9-Smad3/vector group of mice. F FCM analysis of the proportions of CD11b + Ly6G hi cells in the EGFP + CD11b + cells of bone marrow from AAV9-Smad3/vector group of mice. G FCM analysis of the expressions of CD86 in the EGFP + CD11b + cells of bone marrow from AAV9-Smad3/vector group of mice. H Cell numbers in control group, 2 μM SIS3 treatment group, 20 ng/mL Tgfβ1 treatment group and Tgfβ1 + SIS3 treatment group after MΦ induction by 20 ng/mL M-CSF for 7 days and DC induction by 20 ng/mL GM-CSF and 10 ng/mL IL-4 for 9 days. I – K Analyzing DC and MΦ proportions, MHCII and Ki67 expressions, and cellular morphology of each treatment group respectively in DC and MΦ induction system. L Western blot analysis of the Smad3 expressions in initial bone marrow cells (BMC) and BMC-induced MΦ, DC, and MO-MDSC. Except C ( n = 29), error bars of statistical graphs represent mean ± SD, n = 3. For ( A – C , E – G ), p -values were determined using two sides unpaired t-test; For ( D , H – J ), p -values were determined using one-way ANOVA with Tukey test. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns no significant.

Article Snippet: The murine colon cancer cell line CT26 was obtained from Applied Biological Materials Inc. (Zhenjiang, China).

Techniques: Western Blot, Derivative Assay, Plasmid Preparation, Control

A , B Animal imaging analysis of the fluorescence intensity and distribution of EGFP in the organs of mice with injection of Lyz2>Kozak-Smad3-AAV9 and construction of CT26 mouse models for 4 weeks. C Analysis of the tumor growth curve in mice with injection of Lyz2>Kozak-Smad3/EGFP-AAV9 (Lyz2-Smad3 group) or Lyz2>Kozak/EGFP-AAV9 (AAV9-Vector group) during construction of CT26 mouse models for 24 days. D Analysis of the tumor and spleen size in Lyz2-Smad3/Vector group mice after construction of CT26 mouse models for 24 days. E FCM analysis of the proportion of CTL and Treg cells infiltrated in tumor tissues in Lyz2-Smad3/Vector group mice. F FCM analysis of the proportion of CD11b + Ly6G hi PMN-MDSC, CD11b + Ly6C hi MO − MDSC, CD11b + F4/80 hi MΦ, and CD11c + MHCII + DC infiltrated in tumor tissues in Lyz2-Smad3/Vector group mice under EGFP + gate. G FCM analysis of the MHCII expression in EGFP + CD11b + cells in tumor tissues in Lyz2-Smad3/Vector group mice. For ( C , E – G ), n = 6. p -values were determined using two sides unpaired t-test. * p < 0.05.

Journal: Cell Death & Disease

Article Title: Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer

doi: 10.1038/s41419-025-08228-1

Figure Lengend Snippet: A , B Animal imaging analysis of the fluorescence intensity and distribution of EGFP in the organs of mice with injection of Lyz2>Kozak-Smad3-AAV9 and construction of CT26 mouse models for 4 weeks. C Analysis of the tumor growth curve in mice with injection of Lyz2>Kozak-Smad3/EGFP-AAV9 (Lyz2-Smad3 group) or Lyz2>Kozak/EGFP-AAV9 (AAV9-Vector group) during construction of CT26 mouse models for 24 days. D Analysis of the tumor and spleen size in Lyz2-Smad3/Vector group mice after construction of CT26 mouse models for 24 days. E FCM analysis of the proportion of CTL and Treg cells infiltrated in tumor tissues in Lyz2-Smad3/Vector group mice. F FCM analysis of the proportion of CD11b + Ly6G hi PMN-MDSC, CD11b + Ly6C hi MO − MDSC, CD11b + F4/80 hi MΦ, and CD11c + MHCII + DC infiltrated in tumor tissues in Lyz2-Smad3/Vector group mice under EGFP + gate. G FCM analysis of the MHCII expression in EGFP + CD11b + cells in tumor tissues in Lyz2-Smad3/Vector group mice. For ( C , E – G ), n = 6. p -values were determined using two sides unpaired t-test. * p < 0.05.

Article Snippet: The murine colon cancer cell line CT26 was obtained from Applied Biological Materials Inc. (Zhenjiang, China).

Techniques: Imaging, Fluorescence, Injection, Plasmid Preparation, Expressing

A FCM analysis of the MHCII expressions after lentivirus transfection of Smad3/Ctrl (Lv-Smad3/Lv-Ctrl) in tumor MO-MDSC for 5 days within TCCM condition. B Detection of suppressive function of MO-MDSC after Smad3 overexpression to CD8 + T cell proliferation isolated from naïve mice by CFSE labeling assay. C qRT-PCR analysis of the Arg-1 and NOS2 expressions in tumor MO-MDSC after lentivirus-transfection of Smad3/Ctrl (Lv-Smad3/Lv-Ctrl) for 24 h within TCCM condition. D Cell morphology of tumor MO-MDSC treated with or without 2500 U/mL M-CSF for 5 days. E , F FCM analysis of the effects of 2 μM DMSO/SIS3 to the matured MΦ from tumor MO-MDSC within 2500U/mL M-CSF condition for 5 days and cell numbers. G Cell morphology of tumor MO-MDSC treated with or without 2 μM ATRA, 20% TCCM, and 10 ng/mL GM-CSF for 5 days. H , I qRT-PCR and Western blot analysis of the Smad3 expressions in tumor MO-MDSC treated with 2 μM DMSO/ATRA for 24 h and 48 h respectively. J , K FCM analysis of the effects of DMSO/SIS3 to the matured MΦ from tumor MO-MDSC within 2 μM ATRA, 20% TCCM and 10 ng/mL GM-CSF for 5 days and cell numbers. L Diagram of intra-tumoral injection of CMTPX probe labeled 5 × 10 6 Lv-Smad3/Lv-Ctrl tumor MO-MDSC in early CT26 mice (day 8 post-inoculation, tumor volume variation <1 mm 3 ). M Sizes of tumors and spleens in Lv-Smad3/Lv-Ctrl group of mice post five days of adoptive transfer. N Detections of Arg-1 activity and NO concentrations of CMTPX + cells isolated by flow cytometry sorting from tumor tissues of Lv-Smad3/Lv-Ctrl group of mice post five days of adoptive transfer. O FCM analysis of the proportions of MHCII + cells in CMTPX + CD45 + CD11b + gate in tumor tissues after Lv-Smad3/Lv - Ctrl tumor MO-MDSC injected for 5 days. P , Q FCM analysis of the proportions of MDSC and F4/80 + cells in CMTPX + CD45 + CD11b + gate , and CD11c + MHCII + DC in CMTPX + CD45 + gate in tumor tissues after Lv-Smad3/Lv − Ctrl tumor MO-MDSC injected for 5 days. R FCM analysis of the expressions of CD206 and iNOS within CMTPX + CD45 + CD11b + F4/80 + cells in tumor tissues after Lv-Smad3/Lv − Ctrl tumor MO-MDSC injected for 5 days. For ( A , H , J , K ), n = 3; For ( B , E , F , N , O , Q , R ), n = 4; For ( C ), n = 6. p -values were determined using two sides unpaired t-test. * p < 0.05; *** p < 0.001; **** p < 0.0001; ns no significant.

Journal: Cell Death & Disease

Article Title: Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer

doi: 10.1038/s41419-025-08228-1

Figure Lengend Snippet: A FCM analysis of the MHCII expressions after lentivirus transfection of Smad3/Ctrl (Lv-Smad3/Lv-Ctrl) in tumor MO-MDSC for 5 days within TCCM condition. B Detection of suppressive function of MO-MDSC after Smad3 overexpression to CD8 + T cell proliferation isolated from naïve mice by CFSE labeling assay. C qRT-PCR analysis of the Arg-1 and NOS2 expressions in tumor MO-MDSC after lentivirus-transfection of Smad3/Ctrl (Lv-Smad3/Lv-Ctrl) for 24 h within TCCM condition. D Cell morphology of tumor MO-MDSC treated with or without 2500 U/mL M-CSF for 5 days. E , F FCM analysis of the effects of 2 μM DMSO/SIS3 to the matured MΦ from tumor MO-MDSC within 2500U/mL M-CSF condition for 5 days and cell numbers. G Cell morphology of tumor MO-MDSC treated with or without 2 μM ATRA, 20% TCCM, and 10 ng/mL GM-CSF for 5 days. H , I qRT-PCR and Western blot analysis of the Smad3 expressions in tumor MO-MDSC treated with 2 μM DMSO/ATRA for 24 h and 48 h respectively. J , K FCM analysis of the effects of DMSO/SIS3 to the matured MΦ from tumor MO-MDSC within 2 μM ATRA, 20% TCCM and 10 ng/mL GM-CSF for 5 days and cell numbers. L Diagram of intra-tumoral injection of CMTPX probe labeled 5 × 10 6 Lv-Smad3/Lv-Ctrl tumor MO-MDSC in early CT26 mice (day 8 post-inoculation, tumor volume variation <1 mm 3 ). M Sizes of tumors and spleens in Lv-Smad3/Lv-Ctrl group of mice post five days of adoptive transfer. N Detections of Arg-1 activity and NO concentrations of CMTPX + cells isolated by flow cytometry sorting from tumor tissues of Lv-Smad3/Lv-Ctrl group of mice post five days of adoptive transfer. O FCM analysis of the proportions of MHCII + cells in CMTPX + CD45 + CD11b + gate in tumor tissues after Lv-Smad3/Lv - Ctrl tumor MO-MDSC injected for 5 days. P , Q FCM analysis of the proportions of MDSC and F4/80 + cells in CMTPX + CD45 + CD11b + gate , and CD11c + MHCII + DC in CMTPX + CD45 + gate in tumor tissues after Lv-Smad3/Lv − Ctrl tumor MO-MDSC injected for 5 days. R FCM analysis of the expressions of CD206 and iNOS within CMTPX + CD45 + CD11b + F4/80 + cells in tumor tissues after Lv-Smad3/Lv − Ctrl tumor MO-MDSC injected for 5 days. For ( A , H , J , K ), n = 3; For ( B , E , F , N , O , Q , R ), n = 4; For ( C ), n = 6. p -values were determined using two sides unpaired t-test. * p < 0.05; *** p < 0.001; **** p < 0.0001; ns no significant.

Article Snippet: The murine colon cancer cell line CT26 was obtained from Applied Biological Materials Inc. (Zhenjiang, China).

Techniques: Transfection, Over Expression, Isolation, Labeling, Quantitative RT-PCR, Western Blot, Injection, Adoptive Transfer Assay, Activity Assay, Flow Cytometry

( A ) MeRIP-qPCR analysis of the m 6 A levels on Smad3 mRNA in BMC, BM-MO-MDSC and MO-MDSC derived from CT26 tumor models. ( B ) qRT-PCR analysis of the Smad3 expressions in tumor MO-MDSC treated with 5 μM DMSO/STM2457 for 24 hours. ( C ) Western blot analysis of the Smad3 expressions in tumor MO-MDSC with or without 5 μM STM2457 treatment for 6/12/24/48/72 hours. ( D ) MeRIP-qPCR analysis of the m 6 A levels on Smad3 mRNA in tumor MO-MDSC under siNC/siMettl3 treatment for 48 hours. ( E ) qRT-PCR analysis of the Smad3 expressions in tumor MO-MDSC treated with siNC/siMettl3 for 48 hours. ( F ) qRT-PCR analysis of the Smad3 expressions in tumor MO-MDSC treated with Lv-Ctrl/Lv-Smad3 for 48 hours. ( G ) Western blot analysis of the Mettl3 expression in initial bone marrow cells (BMC) and bone marrow induced MO-MDSC by TCCM (BM-MO-MDSC). ( H ) Western blot analysis of the Mettl3 expressions in wide-type mice-derived pMΦ, tumor-derived MO-MDSC and wide-type mice-derived CD11b + Ly6C + cells. ( I ) FCM analysis of the proportions of MΦ after 5 μM DMSO/STM2457 treatment for 5 days of tumor MO-MDSC in 10ng/mL M-CSF-condition. ( J ) FCM analysis of the proportions of DC after 5 μM DMSO/STM2457 treatment for 5 days of tumor MO-MDSC in 10 ng/mL GM-CSF and 2.5 ng/mL IL-4 condition. ( K ) The mRNA decay curve of Smad3 in tumor MO-MDSC treated with siNC/siMettl3 after Actinomycin D treatment through qRT-PCR data. ( L ) Plasmids diagram containing wild type or mutated versions of m6A sites 3037 A > C and/or 4591 A > C in the Smad3 gene. ( M ) Double luciferase assay analysis of the luciferase activity of five group tumor MO-MDSC transfected corresponding plasmids for 72 hours. ( N ) Double luciferase assay analysis of the luciferase activity of five group tumor MO-MDSC transfected corresponding plasmids for 72 hours with 5 μM DMSO/STM2457. ( O ) RIP-qPCR analysis of the binding of Ythdf2 protein with Smad3 mRNA in tumor MO-MDSC. Except D (n = 5), error bars of statistic graphs represent mean ± SD, n = 3. For A , D , M and O , p values were determined using one-way ANOVA with Tukey test; For B , E , F , I , J and N , p -values were determined using two sides unpaired t-test. * p < 0.05; ** p < 0.01; **** p < 0.0001; ns no significant.

Journal: Cell Death & Disease

Article Title: Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer

doi: 10.1038/s41419-025-08228-1

Figure Lengend Snippet: ( A ) MeRIP-qPCR analysis of the m 6 A levels on Smad3 mRNA in BMC, BM-MO-MDSC and MO-MDSC derived from CT26 tumor models. ( B ) qRT-PCR analysis of the Smad3 expressions in tumor MO-MDSC treated with 5 μM DMSO/STM2457 for 24 hours. ( C ) Western blot analysis of the Smad3 expressions in tumor MO-MDSC with or without 5 μM STM2457 treatment for 6/12/24/48/72 hours. ( D ) MeRIP-qPCR analysis of the m 6 A levels on Smad3 mRNA in tumor MO-MDSC under siNC/siMettl3 treatment for 48 hours. ( E ) qRT-PCR analysis of the Smad3 expressions in tumor MO-MDSC treated with siNC/siMettl3 for 48 hours. ( F ) qRT-PCR analysis of the Smad3 expressions in tumor MO-MDSC treated with Lv-Ctrl/Lv-Smad3 for 48 hours. ( G ) Western blot analysis of the Mettl3 expression in initial bone marrow cells (BMC) and bone marrow induced MO-MDSC by TCCM (BM-MO-MDSC). ( H ) Western blot analysis of the Mettl3 expressions in wide-type mice-derived pMΦ, tumor-derived MO-MDSC and wide-type mice-derived CD11b + Ly6C + cells. ( I ) FCM analysis of the proportions of MΦ after 5 μM DMSO/STM2457 treatment for 5 days of tumor MO-MDSC in 10ng/mL M-CSF-condition. ( J ) FCM analysis of the proportions of DC after 5 μM DMSO/STM2457 treatment for 5 days of tumor MO-MDSC in 10 ng/mL GM-CSF and 2.5 ng/mL IL-4 condition. ( K ) The mRNA decay curve of Smad3 in tumor MO-MDSC treated with siNC/siMettl3 after Actinomycin D treatment through qRT-PCR data. ( L ) Plasmids diagram containing wild type or mutated versions of m6A sites 3037 A > C and/or 4591 A > C in the Smad3 gene. ( M ) Double luciferase assay analysis of the luciferase activity of five group tumor MO-MDSC transfected corresponding plasmids for 72 hours. ( N ) Double luciferase assay analysis of the luciferase activity of five group tumor MO-MDSC transfected corresponding plasmids for 72 hours with 5 μM DMSO/STM2457. ( O ) RIP-qPCR analysis of the binding of Ythdf2 protein with Smad3 mRNA in tumor MO-MDSC. Except D (n = 5), error bars of statistic graphs represent mean ± SD, n = 3. For A , D , M and O , p values were determined using one-way ANOVA with Tukey test; For B , E , F , I , J and N , p -values were determined using two sides unpaired t-test. * p < 0.05; ** p < 0.01; **** p < 0.0001; ns no significant.

Article Snippet: The murine colon cancer cell line CT26 was obtained from Applied Biological Materials Inc. (Zhenjiang, China).

Techniques: Derivative Assay, Quantitative RT-PCR, Western Blot, Expressing, Luciferase, Activity Assay, Transfection, Binding Assay

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