Journal: Nature Communications

Article Title: Paclitaxel drives TREM2 + macrophage expansion underlying its inferior therapeutic efficacy compared to Nab-paclitaxel

doi: 10.1038/s41467-026-69060-5

Figure Lengend Snippet: a Schematic of the experimental setup with THP1 or Raw264.7 cells with indicated treatment. Created in BioRender. Xing, Y. (2026) https://BioRender.com/nsp747p b Quantification of proportion of TREM2 in THP1 and Raw264.7 cells with PTX. n = 3 biological independent samples. c Western blot of THP1 and Raw264.7 cells with indicated treatments. The experiment was independently repeated three times with similar results. d Schematic of the experimental strategy. CM was collected from tumor cells with the indicated treatment. TREM2 expression in macrophages incubated with the CM was assessed. Created in BioRender. Xing, Y. (2026) https://BioRender.com/nsp747p e Quantification of proportion of TREM2 in THP1 incubated with CM of BT549 cells, SUM159 cells and MDA-MB-231 cells treated with PTX, in BMDM incubated with CM of Py8119 treated with PTX, in Raw264.7 incubated with CM from 4T1 and Py8119 cells treated with PTX, respectively. n = 3 biological independent samples. f Western blot analysis of TREM2 and related proteins in THP1, BMDMs, and Raw264.7 cells incubated with CM from BT549, SUM159, Py8119, and 4T1 cells, respectively. The experiment was independently repeated three times with similar results. g Representative immunofluorescence staining of THP1 cells incubated with BT549 CM. n = 3 biological independent samples. h Quantification of proportion of TREM2 in THP1 incubated with CM from BT549, SUM159, and MDA-MB-231 cells treated with Nab-PTX, respectively. n = 3 biological independent samples. i Quantification of the proportion of TREM2 in BMDM incubated with CM of Py8119 treated with Nab-PTX. n = 3 biological independent samples. j Cytokine array analysis of CM from BT549 cells treated indicated treatment. k Western blot analysis of the indicated proteins in Raw264.7 cells and BMDMs treated with recombinant FGF2. The experiment was independently repeated three times with similar results. l Quantification of the proportion of TREM2 in Raw264.7 cells and BMDMs treated with recombinant FGF2. n = 3 biological independent samples. m Schematic of the experimental strategy. CM was collected from tumor cells with the indicated treatment, and then pretreatment using an FGF2 neutralizing antibody. TREM2 expression in macrophages incubated with the CM was assessed. Created in BioRender. Xing, Y. (2026) https://BioRender.com/nsp747p n Western blot analysis of the indicated proteins in Raw264.7 and BMDMs incubated with the indicated CM. The experiment was independently repeated three times with similar results. o Quantification of the proportion of TREM2 in Raw264.7 and BMDMs incubated with the indicated CM. n = 3 biological independent samples. p Representative multiplex immunofluorescence staining of CD68, TREM2 and FGF2 in tumors treated with PTX or Nab-PTX ( n = 3 mice per group). The experiment was independently repeated three times with similar results. Data are shown as means ± S.D. and were analyzed by two-sided unpaired Student’s t test ( b , e , h and i ) and two-sided one-way ANOVA followed by Tukey’s test ( l and o ). Source data are provided as a Source Data file.

Article Snippet: The FGF2 protein (HY-P73052AF) was purchased from MedChemExpress and used with indicated concentration.

Techniques: Western Blot, Expressing, Incubation, Immunofluorescence, Staining, Recombinant, Multiplex Assay

Journal: Nature Communications

Article Title: Paclitaxel drives TREM2 + macrophage expansion underlying its inferior therapeutic efficacy compared to Nab-paclitaxel

doi: 10.1038/s41467-026-69060-5

Figure Lengend Snippet: a Overlap of RNA-seq ( n = 3) and PROMO public database analyses to predict transcription factors regulating TREM2 expression. b Correlations between FGF2 and ATF3 expression in breast cancer using TCGA databases. c qPCR analysis of Atf3 expression in the indicated cells. n = 4 (DMSO and PTX) or 3 (PBS and Nab-PTX) biological independent samples. d Western blot analysis of the indicated proteins in Py8119 cells transfected with ATF3-expressing or control vectors. The experiment was independently repeated three times with similar results. e qPCR analysis of Fgf2 expression in Py8119 cells transfected with Atf3 -expressing or control vectors. n = 3 biological independent samples. f Luciferase activity in HEK293T cells transfected with the indicated reporters and Atf3 -expressing or control vectors. n = 3 biological independent samples. g Abundance of Atf3 bound to the Trem2 promoter in Py8119 cells, as assessed by ChIP-qPCR. n = 3 biological independent samples. h ATAC-seq tracks showing the chromatin accessibility in the ATF3 loci for BT549 cells treated by PTX or Nab-PTX. n = 2 samples per group. Data are shown as means ± S.D. and were analyzed by two-sided unpaired Student’s t test ( c, e and f ) and two-sided two-way ANOVA followed by Šídák’s test ( g ). Source data are provided as a Source Data file.

Article Snippet: The FGF2 protein (HY-P73052AF) was purchased from MedChemExpress and used with indicated concentration.

Techniques: RNA Sequencing, Expressing, Western Blot, Transfection, Control, Luciferase, Activity Assay, ChIP-qPCR

Journal: Nature Communications

Article Title: Paclitaxel drives TREM2 + macrophage expansion underlying its inferior therapeutic efficacy compared to Nab-paclitaxel

doi: 10.1038/s41467-026-69060-5

Figure Lengend Snippet: a Overlap of GeneCards and EDCODE public databases analyses to predict transcription factors that regulate TREM2. b Western blot analysis of the indicated proteins in BMDMs and Raw264.7 cells incubated with FGF2 (left) and with CM from Py8119 cells treated with PTX (right). The experiment was independently repeated three times with similar results. c Western blot analysis of the indicated proteins in Raw264.7 cells incubated with the indicated treatment. The experiment was independently repeated three times with similar results. d qPCR analysis of Trem2 expression in BMDMs transfected with Egr1 -expressing vectors. n = 3 biological independent samples. e Western blot analysis of TREM2 expression in BMDMs transfected with Egr1 -expressing vectors. The experiment was independently repeated three times with similar results. f Luciferase activity of HEK293T cells transfected with the indicated reporters and EGR1 -expressing or control vectors. n = 3 biological independent samples. g Abundance of EGR1 bound to the TREM2 promoter in BMDMs assessed by ChIP-qPCR. n = 3 biological independent samples. h Schematic of the Transwell assay. The first CM was collected from tumor cells with indicated treatment, and the second CM was collected from macrophages incubated with the first CM. The migration and invasion capabilities of macrophages incubated with the first CM were assessed. Created in BioRender. Xing, Y. (2026) https://BioRender.com/nsp747p i Quantification of migration and invasion of Py8119 cells induced by BMDM CM incubated with CM from Py8119 cells treated with PTX, and BT549, SUM159, and MDA-MB-231 cells induced by THP1 CM incubated with CM from BT549, SUM159, and MDA-MB-231 cells treated with PTX (left) or Nab-PTX (right), respectively. n = 5 biological independent samples. j Cytokine array analysis of CM from BMDMs with or without TREM2. k Quantification of migration and invasion of Py8119 cells incubated with indicated proteins. n = 3 biological independent samples. l Quantification of migration and invasion of Py8119 cells induced by CM from BMDMs ( Trem2 +/+ ) with CDE-096. n = 3 biological independent samples. m Western blot analysis of EMT- stimulating proteins in BMDMs incubated with indicated proteins. The experiment was independently repeated three times with similar results. n Schematic illustration showing that FGF2 promotes ERK1/2 phosphorylation to upregulate EGR1, which increases TREM2 expression in macrophages. Upregulated TREM2 enhances the secretion of Serpin E1, HGF, CCL3, and CXCL2 from macrophages to tumor cells, facilitating tumor metastasis via EMT. Created in BioRender. Xing, Y. (2026) https://BioRender.com/nsp747p . Data are shown as means ± S.D. and were analyzed by two-sided unpaired Student’s t test ( d, f, i and l ), two-sided one-way ANOVA followed by Tukey’s test ( k ) and two-sided two-way ANOVA followed by Šídák’s test ( g ). Source data are provided as a Source Data file.

Article Snippet: The FGF2 protein (HY-P73052AF) was purchased from MedChemExpress and used with indicated concentration.

Techniques: Western Blot, Incubation, Expressing, Transfection, Luciferase, Activity Assay, Control, ChIP-qPCR, Transwell Assay, Migration, Phospho-proteomics

Journal: Nature Communications

Article Title: Paclitaxel drives TREM2 + macrophage expansion underlying its inferior therapeutic efficacy compared to Nab-paclitaxel

doi: 10.1038/s41467-026-69060-5

Figure Lengend Snippet: PTX, but not Nab-PTX, promotes lung metastasis by inducing TREM2 + macrophage recruitment. Mechanistically, PTX enhances the ATF3-FGF2 axis in breast cancer cells; secreted FGF2 activates the EGR1–TREM2–EMT cytokine axis in macrophages. Created in BioRender. Xing, Y. (2026) https://BioRender.com/6hxlbow .

Article Snippet: The FGF2 protein (HY-P73052AF) was purchased from MedChemExpress and used with indicated concentration.

Techniques:

Journal: Cell Transplantation

Article Title: c-Casitas b-Lineage Lymphoma Downregulation Improves the Ability of Long-term Cultured Mesenchymal Stem Cells for Promoting Angiogenesis and Diabetic Wound Healing

doi: 10.1177/0963689721989605

Figure Lengend Snippet: The migration and angiogenic factors paracrine activity were decreased in long-term cultured MSCs and increased by treating with c-Cbl LNA Gapmers. (A) HUVECs were suspended in EC complete medium (PC) or vehicle (NC)-, P3 MSCs-, P10 MSCs-P10 + scramble LNA Gapmers (P10 + SCR) MSCs-, P10 + c-Cbl LNA Gapmers (P10 + c-Cbl KD) MSCs-conditioned EC basal medium supplemented with 0.75% FBS, and incubated for 8 h (original magnification, 10×) ( n = 3). The tube length, nodes, and meshes in different groups counted in three fields per well were statistically analyzed by histogram analysis. (B) The VEGFA, HGF, and bFGF level in the conditioned media were assessed by ELISA assay ( n = 3). (C) The representative picture and histogram analysis of the stained MSCs migrated to the bottom surface of the upper chamber with 10× magnification in each group ( n = 3). Error bars represent the mean ± SE. # P < 0.05 compared with the NC group and * P < 0.05 versus between the indicated groups. bFGF: basic fibroblast growth factor; c-Cbl: c-Casitas b-lineage lymphoma; EC: endothelial cell; HGF: hepatocyte growth factor; HUVEC: human umbilical vein endothelial cell; LNA Gapmers: locked nucleic acid–modified antisense oligonucleotide gapmers; MSC: mesenchymal stem cell; NC: negative control; PC: positive control; SE: standard error; VEGFA: vascular endothelial growth factor A.

Article Snippet: The supernatant was absorbed and the amount of angiogenic factors was analyzed by vascular endothelial growth factor A (VEGFA) ELISA kit (BOSTER Biological Technology, Wuhan, China), basic fibroblast growth factor (bFGF) ELISA kit (Cusabio Biotech, Wuhan, China), and hepatocyte growth factor (HGF) ELISA kit (BOSTER Biological Technology, Wuhan, China) according to the manufacturer’s instructions.

Techniques: Migration, Activity Assay, Cell Culture, Incubation, Enzyme-linked Immunosorbent Assay, Staining, Modification, Negative Control, Positive Control

Journal: bioRxiv

Article Title: Endotome as a Source of Human Peri-Aortic Brown Adipocytes

doi: 10.64898/2026.07.04.735132

Figure Lengend Snippet: (A) UMAP showing the identified subtypes of (top) day-6 somite and (bottom) day-8 endotome cells. End. Pro., endotome progenitors. VE, vascular endothelial cells. vSMC, vascular smooth muscle cell. (B) Featureplots showing representative markers of somite identity ( PAX3 ), endotome identity ( EBF2 ) and TGF-β signaling pathway ( TGFBR2 , SMAD3 , TGFBI ). (C) Stack plots showing the proportions of identified cell types in (left) day-6 somite and (right) day-8 endotome cultures. Colors and annotations are the same as in (A). (D) Dotplot displaying a curated list of marker genes delineating identified cell types in (A). Fraction of detected cells below 1% were omitted. (E) Mean (top) and rank-ordered (bottom) CUT&Tag signal intensities for EBF2 and H3K27ac at putative enhancer regions in endotome cells. (F) Genome browser tracks showing CUT&Tag signals for EBF2 and H3K27ac (putative enhancer marker) in day-6 somite and day-8 endotome cells. Shaded areas in yellow highlighted EBF2-bound putative enhancers in endotome cells. (G) Dotplot showing scaled expression of core WNT pathway genes in day-6 somite (d6) and day-8 endotome (d8) cells. Cells analyzed were from (A). (H) Lipid (Oil Red O) staining results showing lipid formation on day 33, under conditions where endotome cells were subjected to 4 days of WNT activation (CHIR-99021) or inhibition (IWP-2 and XAV-939). Blank control was treated with basic medium containing FGF2 and ITS only. Experiments were reproduced in more than three biological batches. (I) Quantification of lipid-stain positive areas in BA cultures in (H). n = 8. Data were presented as mean ± SEM. *p < 0.05, ***p < 0.001. ns, no statistical significance. (J) Real-time qPCR analysis of UCP1 , PPARG and ADIPOQ in BA cultures as shown (H). Data were presented as mean ± SEM. n = 3. *p < 0.05, ****p < 0.0001. (K) Left, representative images of UCP1-tagGFP in day-33 BA cultures with (CHIR-99021) or without (blank) 4 days of WNT activation. Right, fraction of UCP1-tagGFP positive cells in relative to DAPI stained cells. n = 8. Data were presented as mean ± SEM. ***p < 0.001.

Article Snippet: The complete HAIF was reconstituted by supplementing the basic defined medium (DM ) with 10 ng/mL human Heregulin β1 (Qkine, QK045), 10 ng/mL human Activin A (Qkine, QK001), 8 ng/mL human FGF2 G3 form (Qkine, QK052) and 200 ng/mL human IGF-1 LR3 form (Qkine, QK041).

Techniques: Marker, Expressing, Staining, Activation Assay, Inhibition, Control