Journal: Stem Cell Research & Therapy

Article Title: iRGD-modified 3D exosomes delivered miR-99b-5p induces ferroptosis to inhibit colorectal cancer progression by regulating FGFR3/PI3K/AKt pathway

doi: 10.1186/s13287-026-05129-8

Figure Lengend Snippet: The 3D-Exo-miR-99b-5p derived from MSCs promotes ferroptosis and suppresses FGFR3/PI3K/AKt pathway in CRC cells. A–B TEM micrographs of LoVo and SW480 cells treated with Erastin and DMSO, red arrow indicated the morphological change of mitochondria. (C) Western blot assay of GPX4 expression in LoVo and SW480 cells. D The levels of Fe 2+ , GSH, ROS and GPX4 in LoVo and SW480 cells detected by ELISA and immunofluorescence ( n = 3). E–F The expression of FGFR3 in LoVo and SW480 cells assessed by western blot assay ( n = 3); G–H Western blot assay of PI3K, p-PI3K, AKt, and p-AKt expression levels in CRC cells co-cultured with 3D-Exo-miR-99b-5p ( n = 3). I–P Verification of overexpression (OE) and knockdown (Si) of FGFR3 in LoVo and SW480 cells through Real-time PCR and western blot assay ( n = 3). Q–R Western blot assay of PI3K, p-PI3K, AKt, and p-AKt expression in CRC cells transfected with OE- or Si-FGFR3 vectors ( n = 3). Student’s t-test was used to compare two groups, while one-way ANOVA followed by Tukey’s post hoc test was used for comparisons between three groups. Data are presented as means ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: To investigate the mechanisms involved in ferroptosis, cells were treated with the ferroptosis inducer Erastin (Cat. No. HY-15763, MCE), the ferroptosis inhibitor ferrostatin-1 (Cat. No. HY-100579, MCE, New Jersey, USA), the pyroptosis inhibitor Z-VAD-FMK (Cat. No. A834991, AmBeed, Shanghai, China), the RIP1 inhibitor Necrostatin-1 (Cat. No. A181851, AmBeed), the PI3K signaling pathway inhibitor LY294002 (Cat. No. HY-10108, MCE), and the PI3K signaling pathway activator 740Y-P (Cat. No. HY-P0175, MCE).

Techniques: Derivative Assay, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Cell Culture, Over Expression, Knockdown, Real-time Polymerase Chain Reaction, Transfection

Journal: Stem Cell Research & Therapy

Article Title: iRGD-modified 3D exosomes delivered miR-99b-5p induces ferroptosis to inhibit colorectal cancer progression by regulating FGFR3/PI3K/AKt pathway

doi: 10.1186/s13287-026-05129-8

Figure Lengend Snippet: The 3D-Exo-miR-99b-5p regulates the ferroptosis process by inhibiting the PI3K/AKt pathway. A–B Western blot analysis of PI3K, p-PI3K, AKt, and p-AKt expression levels in CRC cells after treatment with Erastin or combined with Fer-1 ( n = 3). C–J The levels of Fe 2+ , GSH, and ROS in LoVo and SW480 cells detected by ELISA and immunofluorescence ( n = 3). K–L Western blot assay of GPX4 expression in LoVo and SW480 cells ( n = 3). One-way ANOVA followed by Tukey’s post hoc test was used for comparisons between three groups. Data are presented as means ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: To investigate the mechanisms involved in ferroptosis, cells were treated with the ferroptosis inducer Erastin (Cat. No. HY-15763, MCE), the ferroptosis inhibitor ferrostatin-1 (Cat. No. HY-100579, MCE, New Jersey, USA), the pyroptosis inhibitor Z-VAD-FMK (Cat. No. A834991, AmBeed, Shanghai, China), the RIP1 inhibitor Necrostatin-1 (Cat. No. A181851, AmBeed), the PI3K signaling pathway inhibitor LY294002 (Cat. No. HY-10108, MCE), and the PI3K signaling pathway activator 740Y-P (Cat. No. HY-P0175, MCE).

Techniques: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence

Journal: Stem Cell Research & Therapy

Article Title: iRGD-modified 3D exosomes delivered miR-99b-5p induces ferroptosis to inhibit colorectal cancer progression by regulating FGFR3/PI3K/AKt pathway

doi: 10.1186/s13287-026-05129-8

Figure Lengend Snippet: Targeted anti-tumor therapy of iRGD-Exo-miR-99b-5p in vivo. A Fluorescent images of whole-body imaging of tumor-bearing mice after treatment with DiR-labeled exosomes ( n = 3). B Representative images of ex vivo fluorescent signals in the major organs at two days after the last injection ( n = 3). C–D Cell viability measured by CCK8 assay after three different treatments in LoVo and SW480 cells ( n = 3). Quantitation of synergism and antagonism in iRGD-Exo-miR-99b-5p and 5-FU combination. Fa versus CI plots were generated by CompuSyn. CI > 1, antagonism; CI < 1, synergy; CI = 1, additivity. E–G The tumor weight and volume of mice in each group ( n = 5). H Body weight changes in tumor-bearing mice in each group ( n = 5). I HE staining and IHC staining of Ki67 in tumor tissues ( n = 5). J IHC score for Ki-67 staining in each group ( n = 5). K Changes of Fe 2+ , ROS, GSH and GPX expression in tumor tissues of each group ( n = 5). L–M Changes of FGFR3, P-PI3K, PI3K, p-AKt, and AKt expression in tumor tissues of each group ( n = 3). One-way ANOVA followed by Tukey’s post hoc test was used for comparisons between three groups. Data are presented as means ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: To investigate the mechanisms involved in ferroptosis, cells were treated with the ferroptosis inducer Erastin (Cat. No. HY-15763, MCE), the ferroptosis inhibitor ferrostatin-1 (Cat. No. HY-100579, MCE, New Jersey, USA), the pyroptosis inhibitor Z-VAD-FMK (Cat. No. A834991, AmBeed, Shanghai, China), the RIP1 inhibitor Necrostatin-1 (Cat. No. A181851, AmBeed), the PI3K signaling pathway inhibitor LY294002 (Cat. No. HY-10108, MCE), and the PI3K signaling pathway activator 740Y-P (Cat. No. HY-P0175, MCE).

Techniques: In Vivo, Imaging, Labeling, Ex Vivo, Injection, CCK-8 Assay, Quantitation Assay, Generated, Staining, Immunohistochemistry, Expressing

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Expressing, Western Blot, CCK-8 Assay

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the proliferation and glycolysis of glioma cells by mediating the PTEN-PI3K/AKT pathway.Cell viability of various groups in U87 and U251 cell lines (A); detection of glucose (GLU) and lactate (LA) levels in the culture supernatant of various groups in U87 and U251 cell lines using biochemical assay kits (B); qPCR was used to detect the mRNA levels of GLUT1 and HK2 in various groups of U87 and U251 cell lines (C). Statistical significance *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001,"ns" P ≥ 0.05.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques:

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the PTEN-PI3K/AKT pathway in glioma xenografts.Western blotting was used to detect the protein expression levels of PTEN, PI3K, p-AKT, and AKT in cells from each group.* P < 0.05 vs TNKS1-siRNA NC, @ P < 0.05 vs TNKS1-siRNA，# P < 0.05 vs Inhibitor.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Western Blot, Expressing

Journal: Biochemistry and Biophysics Reports

Article Title: Salvianolic acid B mitigates senescence and promotes osteogenesis of senescent bone marrow mesenchymal stem cells via the PI3K/AKT pathway

doi: 10.1016/j.bbrep.2026.102624

Figure Lengend Snippet: Sal-B Exerts the Therapeutic Effects by Modulating the PI3K/AKT Pathway. (A) Western blot of PI3K, p-PI3K, AKT, and p -AKT proteins in the BMSCs of the different treatment groups. (B-E) Quantitative data for relevant protein expression normalized to β-Actin. (F and G) The mRNA expression of PIK3CA and AKT1 in BMSCs by qRT-PCR. (I) Western blot of ALP, Runx2, P21 and P16 proteins in BMSCs of the different treatment groups. (Sal-B concentration: 100 μmol; LY294002 concentration: 10 μM; n = 3). (J-M) Quantitative data for relevant protein expression normalized to β-Actin. ∗: P < 0.05; #: P < 0.01.

Article Snippet: To inhibit PI3K or AKT, 10 μM LY294002 (HY-10108; MCE, USA) was used.

Techniques: Western Blot, Expressing, Quantitative RT-PCR, Concentration Assay

Journal: Frontiers in Cell and Developmental Biology

Article Title: Dermal mesenchymal stem cells promote angiogenesis in HMEC-1 via activation of the angiopoietin 1/Tie2 pathway in psoriasis

doi: 10.3389/fcell.2026.1771279

Figure Lengend Snippet: ANGPT1-Overexpressing N-DMSCs Promote HMEC-1 Angiogenesis via the PI3K/AKT Pathway. (A–D) Protein levels of p-PI3K (A,B) and p-AKT (C,D) in HMEC-1 co-cultured with N-DMSCs transfected with pLVX-ANGPT1 high (with or without LY294002 treatment) detected by Western blotting. (E) HMEC-1 viability measured by CCK-8 assay. (F,G) Percentage of EdU-positive HMEC-1 cells (scale bar = 100 μm). (H,I) Numbers of migrated HMEC-1 detected by Transwell assay (scale bar = 50 μm). (J) Phase-contrast micrographs of vascular-like structures formed by HMEC-1 (scale bar = 200 μm), and quantitative analysis of nodes (K) , meshes (L) , junctions (M) , and branches (N) of vascular-like structures. (O) mRNA levels of proliferation-related genes (Ki67, CCND1), migration-related genes (RAC1), and angiogenesis-related genes (VEGFA) analyzed by qRT-PCR. (P,Q) Protein levels of proliferation-related genes (Cyclin D1, Cdk2) and angiogenesis-related genes (VEGFA) detected by Western blotting. All protein levels normalized to β-actin. All experiments were performed in triplicate (n = 6 per group). ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Depending on the experimental group, Tie2 kinase inhibitor (Tie2i, Abcam, UK), angiogenesis inhibitor (KYP-2047, MCE, USA), Tie2 activator (AKB-9778, MCE, USA), PI3K inhibitor (LY294002, MCE, USA), PI3K activator (740 Y-P, MCE, USA), MEK inhibitor (PD98059, MCE, USA) or STAT3 inhibitor (Stattic, MCE, USA) was added to the medium.

Techniques: Cell Culture, Transfection, Western Blot, CCK-8 Assay, Transwell Assay, Migration, Quantitative RT-PCR

Journal: Frontiers in Cell and Developmental Biology

Article Title: Dermal mesenchymal stem cells promote angiogenesis in HMEC-1 via activation of the angiopoietin 1/Tie2 pathway in psoriasis

doi: 10.3389/fcell.2026.1771279

Figure Lengend Snippet: ANGPT1-Knockdown P-DMSCs Inhibit HMEC-1 Angiogenesis via the PI3K/AKT Pathway. (A–D) Protein levels of p-PI3K (A,B) and p-AKT (C,D) in HMEC-1 co-cultured with P-DMSCs transfected with pLKO.1-shANGPT1 (with or without 740 Y-P treatment) detected by Western blotting. (E) HMEC-1 viability measured by CCK-8 assay. (F,G) Percentage of EdU-positive HMEC-1 cells (scale bar = 100 μm). (H,I) Numbers of migrated HMEC-1 detected by Transwell assay (scale bar = 50 μm). (J) Phase-contrast micrographs of vascular-like structures formed by HMEC-1 (scale bar = 200 μm), and quantitative analysis of nodes (K) , meshes (L) , junctions (M) , and branches (N) of vascular-like structures. (O) mRNA levels of proliferation-related genes (Ki67, CCND1), migration-related genes (RAC1), and angiogenesis-related genes (VEGFA) analyzed by qRT-PCR. (P,Q) Protein levels of Cyclin D1 and VEGFA detected by Western blotting. All protein levels normalized to β-actin. All experiments were performed in triplicate (n = 6 per group). ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Depending on the experimental group, Tie2 kinase inhibitor (Tie2i, Abcam, UK), angiogenesis inhibitor (KYP-2047, MCE, USA), Tie2 activator (AKB-9778, MCE, USA), PI3K inhibitor (LY294002, MCE, USA), PI3K activator (740 Y-P, MCE, USA), MEK inhibitor (PD98059, MCE, USA) or STAT3 inhibitor (Stattic, MCE, USA) was added to the medium.

Techniques: Knockdown, Cell Culture, Transfection, Western Blot, CCK-8 Assay, Transwell Assay, Migration, Quantitative RT-PCR

Journal: Frontiers in Cell and Developmental Biology

Article Title: Dermal mesenchymal stem cells promote angiogenesis in HMEC-1 via activation of the angiopoietin 1/Tie2 pathway in psoriasis

doi: 10.3389/fcell.2026.1771279

Figure Lengend Snippet: A schematic diagram illustrating the abnormal angiogenesis in the psoriasis lesion microenvironment mediated by the Ang1/Tie2 axis. In the DMSCs of psoriasis patients, the upregulated Ang1 binds to the Tie2 receptor on the surface of HMEC-1 through paracrine secretion, activating the downstream PI3K/AKT pathway, promoting the proliferation, migration and tube formation of HMEC-1, and ultimately leading to abnormal angiogenesis in the dermal papillary layer of psoriasis.

Article Snippet: Depending on the experimental group, Tie2 kinase inhibitor (Tie2i, Abcam, UK), angiogenesis inhibitor (KYP-2047, MCE, USA), Tie2 activator (AKB-9778, MCE, USA), PI3K inhibitor (LY294002, MCE, USA), PI3K activator (740 Y-P, MCE, USA), MEK inhibitor (PD98059, MCE, USA) or STAT3 inhibitor (Stattic, MCE, USA) was added to the medium.

Techniques: Migration