dynamics & pattern formation Search Results


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Revvity dma 8000 analyzer
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fluidigm 48 48 dynamic arraytm integrated fluidic circuit
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Bruker Corporation bruker dynamiccenter2 5 3
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fluidigm array ifc
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Cell Signaling Technology Inc mitochondrial dynamics antibody sampler kit ii
DEHP induced <t>mitochondrial</t> respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).
Mitochondrial Dynamics Antibody Sampler Kit Ii, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fluidigm 192 24 dynamic array platform
DEHP induced <t>mitochondrial</t> respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).
192 24 Dynamic Array Platform, supplied by fluidigm, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Revvity dynamic mechanical analysis dma
DEHP induced <t>mitochondrial</t> respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).
Dynamic Mechanical Analysis Dma, supplied by Revvity, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Gerstel GmbH automated dhs tation
DEHP induced <t>mitochondrial</t> respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).
Automated Dhs Tation, supplied by Gerstel GmbH, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
FRITSCH GmbH ball mill
DEHP induced <t>mitochondrial</t> respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).
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Image Search Results


DEHP induced mitochondrial respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).

Journal: Advanced Science

Article Title: SLC6A14 Drives Mitochondrial Fusion and Oxidative Phosphorylation to Promote Cancer Stemness and Early‐Onset of Breast Cancer

doi: 10.1002/advs.202510811

Figure Lengend Snippet: DEHP induced mitochondrial respiration capacity. A) The enriched metabolic pathways were identified with joint metabolomics and transcriptomics analysis by the Genes and Metabolites (GAM) web service. B) The tomographic image and average total length of mitochondria in parental and DEHP10 of MCF7 cells were captured with the 3D Cell Explorer‐fluo and were quantified with the Smart Mitochondrial Assay LIVE (Nanolive). C) The protein expressions of mitochondria dynamics‐related genes in parental and DEHP‐exposed MCF7 cells were determined in a Western blot with the indicated antibodies. D) Staining of parental cells and DEHP1 of MCF7 and T47D cells with MitoSOX Red was visualized by fluorescence microscopy. E and F) The OCR in parental cells and DEHP‐exposed MCF7 cells was analyzed by Seahorse Metabolic Analyzer following the sequential addition of mitochondrial inhibitors, oligomycin, FCCP, rotenone/antimycin A in (E). Maximal respiration and spare respiratory capacity were calculated in (F). G) Staining of parental and DEHP1 of MCF7 and T47D cells with MitoSOX Red following the 24‐hr treatments with AOA (200 µ m ), Perhexiline (5 µ m ), and 2DG (25 µ m ) was visualized by fluorescence microscopy. H) The growth of parental and DEHP10 of MCF7 cells cultured in matrigel was suppressed by AOA (200 µ m ) or Perhexiline (5 µ m ) for 7 days. I) MCF7/DEHP10 was treated with 2DG (25 µ m ), AOA (200 µ m ), and Perhexiline (5 µ m ) for 48 h, and SOX2 expression was examined in Western blot analysis. J) The growth of patient‐derived organoids (PDO‐1 and PDO‐2) was suppressed by AOA (200 µ m ) and Perhexiline (5 µ m ) but not 2DG (25 µ m ) for 7 days. Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns. not significant; ∗ p < 0.05; ∗∗ p < 0.01 versus the control group. Student's t ‐test (B) and one‐way ANOVA with Tukey's multiple comparisons test (F).

Article Snippet: Antibodies against SOX2 (Santa Cruz; sc‐365823; RRID: AB_10 842 165), CD133 (abcam; ab19898;; RRID: AB_470 302), ERα (Santa Cruz; sc‐8002; RRID: AB_627 558), pERα (Ser108; Cell Signaling; 2511; RRID: AB_331 289), SLC6A14 (Thermo Fisher; PA5‐42452; RRID: AB_2 576 522), SLC38A2 (Medical&Biological Laboratories (MBL); BMP081; RRID: AB_10 597 880), BCRP (Millipore; MAB4146; RRID: AB_2 220 429), mitochondrial dynamics antibody sampler kit II (Cell Signaling; 74 792), mitochondrial marker antibody sampler kit (Cell Signaling; 8674; RRID: AB_11 217 817), β‐actin (Sigma‐Aldrich; A2228; RRID: AB_476 697) and α‐Tubulin (Sigma‐Aldrich; T5168; RRID: AB_477 579) were purchased commercially.

Techniques: Western Blot, Staining, Fluorescence, Microscopy, Cell Culture, Expressing, Derivative Assay, Control

Glutamine transport activity of SLC6A14 is required for mitochondria fusion. A) Parental and DEHP‐exposed MCF7 cells were transfected with SLC6A14 shRNA and cultured in an ultra‐low dish for 7 days, followed by spheroid formation assays. B) Spheroid formation of SLC6A14‐overexpressed MCF7 cells was measured in a 3D cell culture system. C) MCF7 cells were transfected with SLC6A14 plasmids. The expression of MFF was determined in Western blot analysis. D) MCF7 cells treated with αKG for 48 h were subjected to Western blot analysis of MFF expression. E) Parental and DEHP1 MCF7 cells were pretreated with 2.5 m m αMT in a glutamine‐depleted medium for 3 h and then supplemented with 2 m m glutamine for 4 h. The cell lysates were harvested and subjected to glutamine concentration analysis. n = 3. F,G) Parental and DEHP1 MCF7 cells were treated with 2.5 m m αMT for 48 h followed by staining with MitoSpy (F) and mitochondrial superoxide indicator MitoSOX Red (G). Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 versus the control group, one‐way ANOVA with Tukey's multiple comparisons test (A) and Student's t ‐test (E).

Journal: Advanced Science

Article Title: SLC6A14 Drives Mitochondrial Fusion and Oxidative Phosphorylation to Promote Cancer Stemness and Early‐Onset of Breast Cancer

doi: 10.1002/advs.202510811

Figure Lengend Snippet: Glutamine transport activity of SLC6A14 is required for mitochondria fusion. A) Parental and DEHP‐exposed MCF7 cells were transfected with SLC6A14 shRNA and cultured in an ultra‐low dish for 7 days, followed by spheroid formation assays. B) Spheroid formation of SLC6A14‐overexpressed MCF7 cells was measured in a 3D cell culture system. C) MCF7 cells were transfected with SLC6A14 plasmids. The expression of MFF was determined in Western blot analysis. D) MCF7 cells treated with αKG for 48 h were subjected to Western blot analysis of MFF expression. E) Parental and DEHP1 MCF7 cells were pretreated with 2.5 m m αMT in a glutamine‐depleted medium for 3 h and then supplemented with 2 m m glutamine for 4 h. The cell lysates were harvested and subjected to glutamine concentration analysis. n = 3. F,G) Parental and DEHP1 MCF7 cells were treated with 2.5 m m αMT for 48 h followed by staining with MitoSpy (F) and mitochondrial superoxide indicator MitoSOX Red (G). Images represent one representative experiment from three independent experiments. Data were shown as the mean ± SD. ns, not significant; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 versus the control group, one‐way ANOVA with Tukey's multiple comparisons test (A) and Student's t ‐test (E).

Article Snippet: Antibodies against SOX2 (Santa Cruz; sc‐365823; RRID: AB_10 842 165), CD133 (abcam; ab19898;; RRID: AB_470 302), ERα (Santa Cruz; sc‐8002; RRID: AB_627 558), pERα (Ser108; Cell Signaling; 2511; RRID: AB_331 289), SLC6A14 (Thermo Fisher; PA5‐42452; RRID: AB_2 576 522), SLC38A2 (Medical&Biological Laboratories (MBL); BMP081; RRID: AB_10 597 880), BCRP (Millipore; MAB4146; RRID: AB_2 220 429), mitochondrial dynamics antibody sampler kit II (Cell Signaling; 74 792), mitochondrial marker antibody sampler kit (Cell Signaling; 8674; RRID: AB_11 217 817), β‐actin (Sigma‐Aldrich; A2228; RRID: AB_476 697) and α‐Tubulin (Sigma‐Aldrich; T5168; RRID: AB_477 579) were purchased commercially.

Techniques: Activity Assay, Transfection, shRNA, Cell Culture, Expressing, Western Blot, Concentration Assay, Staining, Control

DEHP exposure promotes cancer stemness and early onset of breast cancer via mitochondrial fusion and glutamine metabolism by upregulating SLC6A14. In response to DEHP exposure, SLC6A14 was upregulated in an ERα‐dependent manner to facilitate glutamine uptake and mitochondrial fusion via MFF suppression. The enhanced glutamine metabolism fuels oxidative phosphorylation and de novo nucleotide biosynthesis to promote cancer stemness, resulting in the early onset and chemoresistance of breast cancer. Targeting SLC6A14 glutamine transporter activity was suggested as a promising therapeutic strategy for EOBC patients.

Journal: Advanced Science

Article Title: SLC6A14 Drives Mitochondrial Fusion and Oxidative Phosphorylation to Promote Cancer Stemness and Early‐Onset of Breast Cancer

doi: 10.1002/advs.202510811

Figure Lengend Snippet: DEHP exposure promotes cancer stemness and early onset of breast cancer via mitochondrial fusion and glutamine metabolism by upregulating SLC6A14. In response to DEHP exposure, SLC6A14 was upregulated in an ERα‐dependent manner to facilitate glutamine uptake and mitochondrial fusion via MFF suppression. The enhanced glutamine metabolism fuels oxidative phosphorylation and de novo nucleotide biosynthesis to promote cancer stemness, resulting in the early onset and chemoresistance of breast cancer. Targeting SLC6A14 glutamine transporter activity was suggested as a promising therapeutic strategy for EOBC patients.

Article Snippet: Antibodies against SOX2 (Santa Cruz; sc‐365823; RRID: AB_10 842 165), CD133 (abcam; ab19898;; RRID: AB_470 302), ERα (Santa Cruz; sc‐8002; RRID: AB_627 558), pERα (Ser108; Cell Signaling; 2511; RRID: AB_331 289), SLC6A14 (Thermo Fisher; PA5‐42452; RRID: AB_2 576 522), SLC38A2 (Medical&Biological Laboratories (MBL); BMP081; RRID: AB_10 597 880), BCRP (Millipore; MAB4146; RRID: AB_2 220 429), mitochondrial dynamics antibody sampler kit II (Cell Signaling; 74 792), mitochondrial marker antibody sampler kit (Cell Signaling; 8674; RRID: AB_11 217 817), β‐actin (Sigma‐Aldrich; A2228; RRID: AB_476 697) and α‐Tubulin (Sigma‐Aldrich; T5168; RRID: AB_477 579) were purchased commercially.

Techniques: Phospho-proteomics, Activity Assay