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slc7a5 lat1  (Proteintech)


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    Proteintech slc7a5 lat1
    (A) Schematic representation of SLC3A2-containing amino acid transporters. (B) MDA-MB-231 and (C) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under complete or Glc starvation media for 24 hours, mRNA was extracted and the levels of SLC3A2, <t>SLC7A5,</t> SLC7A6, SLC7A8 and GAPDH as housekeeping gene were quantified by SYBR-green qPCR. Data are presented as 2 -ΔCT ; mean ± SEM, N=3 independent experiments, ****p < 0.0001 Kruskal-Wallis, Dunn’s multiple comparisons test. (D,E) MDA-MB-231 and (F,G) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under Glc starvation for one or two days, respectively. Cells were fixed and stained with (D,F) Hoechst 33342 (magenta), SLC3A2 (cyan) and Phalloidin Alexa Fluor 555 (grey) or (E,G) Hoechst 33342 (cyan), SLC7A5 (red) and Phalloidin Alexa Fluor 555 (grey). Bar, 20 µm. Images were collected with a ZEISS LSM98O Airyscan2 microscope and analysed by Fiji/lmageJ software. Data are presented as mean ± SEM, N=3 independent experiments (the bigger dots represent mean intensity of each field of view); **p < 0.01, ***p < 0.001 Mann-Whitney test. (H, I) MDA-MB-231 and PANC1 cells were transfected with an siRNA targeting SLC3A2 (3A2), an siRNA targeting SLC7A5 (7A5) or a combination of siRNA targeting SLC3A2 and SLC7A5 (3A2+7A5) and grown on 2mg/ml collagen I under Glc starvation for one or three days, respectively. Metabolites were extracted and analysed by targeted mass spectrometry. N=3 independent experiments.
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    Images

    1) Product Images from "Collagen I promotes cancer cell survival via amino acid import and mTORC1 activation"

    Article Title: Collagen I promotes cancer cell survival via amino acid import and mTORC1 activation

    Journal: bioRxiv

    doi: 10.1101/2025.11.26.690708

    (A) Schematic representation of SLC3A2-containing amino acid transporters. (B) MDA-MB-231 and (C) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under complete or Glc starvation media for 24 hours, mRNA was extracted and the levels of SLC3A2, SLC7A5, SLC7A6, SLC7A8 and GAPDH as housekeeping gene were quantified by SYBR-green qPCR. Data are presented as 2 -ΔCT ; mean ± SEM, N=3 independent experiments, ****p < 0.0001 Kruskal-Wallis, Dunn’s multiple comparisons test. (D,E) MDA-MB-231 and (F,G) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under Glc starvation for one or two days, respectively. Cells were fixed and stained with (D,F) Hoechst 33342 (magenta), SLC3A2 (cyan) and Phalloidin Alexa Fluor 555 (grey) or (E,G) Hoechst 33342 (cyan), SLC7A5 (red) and Phalloidin Alexa Fluor 555 (grey). Bar, 20 µm. Images were collected with a ZEISS LSM98O Airyscan2 microscope and analysed by Fiji/lmageJ software. Data are presented as mean ± SEM, N=3 independent experiments (the bigger dots represent mean intensity of each field of view); **p < 0.01, ***p < 0.001 Mann-Whitney test. (H, I) MDA-MB-231 and PANC1 cells were transfected with an siRNA targeting SLC3A2 (3A2), an siRNA targeting SLC7A5 (7A5) or a combination of siRNA targeting SLC3A2 and SLC7A5 (3A2+7A5) and grown on 2mg/ml collagen I under Glc starvation for one or three days, respectively. Metabolites were extracted and analysed by targeted mass spectrometry. N=3 independent experiments.
    Figure Legend Snippet: (A) Schematic representation of SLC3A2-containing amino acid transporters. (B) MDA-MB-231 and (C) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under complete or Glc starvation media for 24 hours, mRNA was extracted and the levels of SLC3A2, SLC7A5, SLC7A6, SLC7A8 and GAPDH as housekeeping gene were quantified by SYBR-green qPCR. Data are presented as 2 -ΔCT ; mean ± SEM, N=3 independent experiments, ****p < 0.0001 Kruskal-Wallis, Dunn’s multiple comparisons test. (D,E) MDA-MB-231 and (F,G) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under Glc starvation for one or two days, respectively. Cells were fixed and stained with (D,F) Hoechst 33342 (magenta), SLC3A2 (cyan) and Phalloidin Alexa Fluor 555 (grey) or (E,G) Hoechst 33342 (cyan), SLC7A5 (red) and Phalloidin Alexa Fluor 555 (grey). Bar, 20 µm. Images were collected with a ZEISS LSM98O Airyscan2 microscope and analysed by Fiji/lmageJ software. Data are presented as mean ± SEM, N=3 independent experiments (the bigger dots represent mean intensity of each field of view); **p < 0.01, ***p < 0.001 Mann-Whitney test. (H, I) MDA-MB-231 and PANC1 cells were transfected with an siRNA targeting SLC3A2 (3A2), an siRNA targeting SLC7A5 (7A5) or a combination of siRNA targeting SLC3A2 and SLC7A5 (3A2+7A5) and grown on 2mg/ml collagen I under Glc starvation for one or three days, respectively. Metabolites were extracted and analysed by targeted mass spectrometry. N=3 independent experiments.

    Techniques Used: SYBR Green Assay, Staining, Microscopy, Software, MANN-WHITNEY, Transfection, Mass Spectrometry

    MDA-MB-231 (A-D) arid PANC1 (E-H) were transfected with an siRNA targeting SLC3A2 (3A2 si), an siRNA targeting SLC7A5 (7A5 si) or a non-targeting siRNA control (Nt si) and grown on 2 mg/ml collagen I under complete or Glc starvation media for 4 days. Cells were fixed and stained with Hoechst 33342. Images were collected by an ImageXpress micro and analysed by Meta×press software. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001 Mann-Whitney test. (I) MDA-MB-231-GFP cells were transfected with a combination of siRNAs targeting SLC3A2 and SLC7A5 (3A2+7A5 si) or a non­targeting siRNA control (Nt si) for 24 hours, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen I and Geltrex (50:50 ratio) for 3 days under Glc starvation. Images were collected by a Nikon Confocal A1 microscope. Invasion area was quantified with Fiji/lmageJ. Bar, 200 µm. Data are presented as mean ± SEM, N=2 independent experiments. (J) PANC1 cells were transfected as in I, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen land Geltrex (50:50 ratio) for 6 days under Glc starvation. Live images were collected every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=2 independent experiments. (K, L) E0771 mouse tumours organoids were grown in a 3 mg/ml collagen I and Geltrex (50:50) mixture and starved in Glc starvation media for 2 days in the presence or absence of 50 mM D-phenylalanine (D-Phe). Spheroids were imaged live every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001; (l,J,K) Two-way ANOVA, Tukey’s multiple comparisons test; (L) Mann-Whitney test.
    Figure Legend Snippet: MDA-MB-231 (A-D) arid PANC1 (E-H) were transfected with an siRNA targeting SLC3A2 (3A2 si), an siRNA targeting SLC7A5 (7A5 si) or a non-targeting siRNA control (Nt si) and grown on 2 mg/ml collagen I under complete or Glc starvation media for 4 days. Cells were fixed and stained with Hoechst 33342. Images were collected by an ImageXpress micro and analysed by Meta×press software. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001 Mann-Whitney test. (I) MDA-MB-231-GFP cells were transfected with a combination of siRNAs targeting SLC3A2 and SLC7A5 (3A2+7A5 si) or a non­targeting siRNA control (Nt si) for 24 hours, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen I and Geltrex (50:50 ratio) for 3 days under Glc starvation. Images were collected by a Nikon Confocal A1 microscope. Invasion area was quantified with Fiji/lmageJ. Bar, 200 µm. Data are presented as mean ± SEM, N=2 independent experiments. (J) PANC1 cells were transfected as in I, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen land Geltrex (50:50 ratio) for 6 days under Glc starvation. Live images were collected every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=2 independent experiments. (K, L) E0771 mouse tumours organoids were grown in a 3 mg/ml collagen I and Geltrex (50:50) mixture and starved in Glc starvation media for 2 days in the presence or absence of 50 mM D-phenylalanine (D-Phe). Spheroids were imaged live every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001; (l,J,K) Two-way ANOVA, Tukey’s multiple comparisons test; (L) Mann-Whitney test.

    Techniques Used: Transfection, Control, Staining, Software, MANN-WHITNEY, Generated, Microscopy

    (A,C) RNA sequencing data from basal-Like breast tumours (n=135) and normal breast tissue (n=291) or pancreatic adenocarcinoma tumours (n=179) and normal pancreatic tissue (n=171) for the co-expression of SLC3A2 and SLC7A5. *p< 0.05. Data were obtained from gepia2.com. (B) Overall survival of basal-like breast cancer patients with high (red) or low (blue) co­expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (D) Disease free survival of pancreatic adenocarcinoma patients with high (red) or low (blue) co-expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (E,F) RNA sequencing data and ROC analysis for the co-expression of SLC3A2 and SLC7A5 from chemoresistant (Non-responder) and chemosensitive (Responder) breast tumours. (E) p = 1,4e-6, Mann-Whitney test. (D) AUG = 0.628; ROC p value = 2.5e-07. Data were generated in ROCplot.com.
    Figure Legend Snippet: (A,C) RNA sequencing data from basal-Like breast tumours (n=135) and normal breast tissue (n=291) or pancreatic adenocarcinoma tumours (n=179) and normal pancreatic tissue (n=171) for the co-expression of SLC3A2 and SLC7A5. *p< 0.05. Data were obtained from gepia2.com. (B) Overall survival of basal-like breast cancer patients with high (red) or low (blue) co­expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (D) Disease free survival of pancreatic adenocarcinoma patients with high (red) or low (blue) co-expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (E,F) RNA sequencing data and ROC analysis for the co-expression of SLC3A2 and SLC7A5 from chemoresistant (Non-responder) and chemosensitive (Responder) breast tumours. (E) p = 1,4e-6, Mann-Whitney test. (D) AUG = 0.628; ROC p value = 2.5e-07. Data were generated in ROCplot.com.

    Techniques Used: RNA Sequencing, Expressing, MANN-WHITNEY, Generated

    Under Glc starvation, collagen I promoted α2β1 integrin-dependent mTORCI activation in breast and pancreatic cancer cells. Collagen I also increased the membrane levels of the LAT1-4F2hc amino acid transporter heavy chain, SLC3A2 (3A2), and light chain, SLC7A5 (7A5), stimulating amino acid import. This resulted in mTORCI activation and autophagy inhibition, leading to increased survival, proliferation and invasion, in 2D and 3C contexts.
    Figure Legend Snippet: Under Glc starvation, collagen I promoted α2β1 integrin-dependent mTORCI activation in breast and pancreatic cancer cells. Collagen I also increased the membrane levels of the LAT1-4F2hc amino acid transporter heavy chain, SLC3A2 (3A2), and light chain, SLC7A5 (7A5), stimulating amino acid import. This resulted in mTORCI activation and autophagy inhibition, leading to increased survival, proliferation and invasion, in 2D and 3C contexts.

    Techniques Used: Activation Assay, Membrane, Inhibition



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    Image Search Results


    (A) Schematic representation of SLC3A2-containing amino acid transporters. (B) MDA-MB-231 and (C) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under complete or Glc starvation media for 24 hours, mRNA was extracted and the levels of SLC3A2, SLC7A5, SLC7A6, SLC7A8 and GAPDH as housekeeping gene were quantified by SYBR-green qPCR. Data are presented as 2 -ΔCT ; mean ± SEM, N=3 independent experiments, ****p < 0.0001 Kruskal-Wallis, Dunn’s multiple comparisons test. (D,E) MDA-MB-231 and (F,G) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under Glc starvation for one or two days, respectively. Cells were fixed and stained with (D,F) Hoechst 33342 (magenta), SLC3A2 (cyan) and Phalloidin Alexa Fluor 555 (grey) or (E,G) Hoechst 33342 (cyan), SLC7A5 (red) and Phalloidin Alexa Fluor 555 (grey). Bar, 20 µm. Images were collected with a ZEISS LSM98O Airyscan2 microscope and analysed by Fiji/lmageJ software. Data are presented as mean ± SEM, N=3 independent experiments (the bigger dots represent mean intensity of each field of view); **p < 0.01, ***p < 0.001 Mann-Whitney test. (H, I) MDA-MB-231 and PANC1 cells were transfected with an siRNA targeting SLC3A2 (3A2), an siRNA targeting SLC7A5 (7A5) or a combination of siRNA targeting SLC3A2 and SLC7A5 (3A2+7A5) and grown on 2mg/ml collagen I under Glc starvation for one or three days, respectively. Metabolites were extracted and analysed by targeted mass spectrometry. N=3 independent experiments.

    Journal: bioRxiv

    Article Title: Collagen I promotes cancer cell survival via amino acid import and mTORC1 activation

    doi: 10.1101/2025.11.26.690708

    Figure Lengend Snippet: (A) Schematic representation of SLC3A2-containing amino acid transporters. (B) MDA-MB-231 and (C) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under complete or Glc starvation media for 24 hours, mRNA was extracted and the levels of SLC3A2, SLC7A5, SLC7A6, SLC7A8 and GAPDH as housekeeping gene were quantified by SYBR-green qPCR. Data are presented as 2 -ΔCT ; mean ± SEM, N=3 independent experiments, ****p < 0.0001 Kruskal-Wallis, Dunn’s multiple comparisons test. (D,E) MDA-MB-231 and (F,G) PANC1 cells were seeded on 2 mg/ml collagen I (Coll) or plastic (P) under Glc starvation for one or two days, respectively. Cells were fixed and stained with (D,F) Hoechst 33342 (magenta), SLC3A2 (cyan) and Phalloidin Alexa Fluor 555 (grey) or (E,G) Hoechst 33342 (cyan), SLC7A5 (red) and Phalloidin Alexa Fluor 555 (grey). Bar, 20 µm. Images were collected with a ZEISS LSM98O Airyscan2 microscope and analysed by Fiji/lmageJ software. Data are presented as mean ± SEM, N=3 independent experiments (the bigger dots represent mean intensity of each field of view); **p < 0.01, ***p < 0.001 Mann-Whitney test. (H, I) MDA-MB-231 and PANC1 cells were transfected with an siRNA targeting SLC3A2 (3A2), an siRNA targeting SLC7A5 (7A5) or a combination of siRNA targeting SLC3A2 and SLC7A5 (3A2+7A5) and grown on 2mg/ml collagen I under Glc starvation for one or three days, respectively. Metabolites were extracted and analysed by targeted mass spectrometry. N=3 independent experiments.

    Article Snippet: Primary antibodies for Phospho-S6 Ribosomal Protein ser235/236 and LC3A/B were from Cell Signalling; α2 integrin (CD49b)-FITC conjugated and β1 integrin (CD29)-Alexa Fluor 488 conjugated from BioLegend; α2 integrin for Western blotting from BD-bioscience; SLC3A2 (CD98) and SLC7A5 (LAT1) from Proteintech and GAPDH from SANTA CRUZ Biotechnology.

    Techniques: SYBR Green Assay, Staining, Microscopy, Software, MANN-WHITNEY, Transfection, Mass Spectrometry

    MDA-MB-231 (A-D) arid PANC1 (E-H) were transfected with an siRNA targeting SLC3A2 (3A2 si), an siRNA targeting SLC7A5 (7A5 si) or a non-targeting siRNA control (Nt si) and grown on 2 mg/ml collagen I under complete or Glc starvation media for 4 days. Cells were fixed and stained with Hoechst 33342. Images were collected by an ImageXpress micro and analysed by Meta×press software. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001 Mann-Whitney test. (I) MDA-MB-231-GFP cells were transfected with a combination of siRNAs targeting SLC3A2 and SLC7A5 (3A2+7A5 si) or a non­targeting siRNA control (Nt si) for 24 hours, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen I and Geltrex (50:50 ratio) for 3 days under Glc starvation. Images were collected by a Nikon Confocal A1 microscope. Invasion area was quantified with Fiji/lmageJ. Bar, 200 µm. Data are presented as mean ± SEM, N=2 independent experiments. (J) PANC1 cells were transfected as in I, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen land Geltrex (50:50 ratio) for 6 days under Glc starvation. Live images were collected every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=2 independent experiments. (K, L) E0771 mouse tumours organoids were grown in a 3 mg/ml collagen I and Geltrex (50:50) mixture and starved in Glc starvation media for 2 days in the presence or absence of 50 mM D-phenylalanine (D-Phe). Spheroids were imaged live every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001; (l,J,K) Two-way ANOVA, Tukey’s multiple comparisons test; (L) Mann-Whitney test.

    Journal: bioRxiv

    Article Title: Collagen I promotes cancer cell survival via amino acid import and mTORC1 activation

    doi: 10.1101/2025.11.26.690708

    Figure Lengend Snippet: MDA-MB-231 (A-D) arid PANC1 (E-H) were transfected with an siRNA targeting SLC3A2 (3A2 si), an siRNA targeting SLC7A5 (7A5 si) or a non-targeting siRNA control (Nt si) and grown on 2 mg/ml collagen I under complete or Glc starvation media for 4 days. Cells were fixed and stained with Hoechst 33342. Images were collected by an ImageXpress micro and analysed by Meta×press software. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001 Mann-Whitney test. (I) MDA-MB-231-GFP cells were transfected with a combination of siRNAs targeting SLC3A2 and SLC7A5 (3A2+7A5 si) or a non­targeting siRNA control (Nt si) for 24 hours, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen I and Geltrex (50:50 ratio) for 3 days under Glc starvation. Images were collected by a Nikon Confocal A1 microscope. Invasion area was quantified with Fiji/lmageJ. Bar, 200 µm. Data are presented as mean ± SEM, N=2 independent experiments. (J) PANC1 cells were transfected as in I, spheroids were generated by the hanging drop method and embedded in 3 mg/ml collagen land Geltrex (50:50 ratio) for 6 days under Glc starvation. Live images were collected every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=2 independent experiments. (K, L) E0771 mouse tumours organoids were grown in a 3 mg/ml collagen I and Geltrex (50:50) mixture and starved in Glc starvation media for 2 days in the presence or absence of 50 mM D-phenylalanine (D-Phe). Spheroids were imaged live every day by an Olympus E45O microscope. Bar, 250 µm. Data are presented as mean ± SEM, N=3 independent experiments, *p < 0.05, **p < 0.01 and ****p < 0.0001; (l,J,K) Two-way ANOVA, Tukey’s multiple comparisons test; (L) Mann-Whitney test.

    Article Snippet: Primary antibodies for Phospho-S6 Ribosomal Protein ser235/236 and LC3A/B were from Cell Signalling; α2 integrin (CD49b)-FITC conjugated and β1 integrin (CD29)-Alexa Fluor 488 conjugated from BioLegend; α2 integrin for Western blotting from BD-bioscience; SLC3A2 (CD98) and SLC7A5 (LAT1) from Proteintech and GAPDH from SANTA CRUZ Biotechnology.

    Techniques: Transfection, Control, Staining, Software, MANN-WHITNEY, Generated, Microscopy

    (A,C) RNA sequencing data from basal-Like breast tumours (n=135) and normal breast tissue (n=291) or pancreatic adenocarcinoma tumours (n=179) and normal pancreatic tissue (n=171) for the co-expression of SLC3A2 and SLC7A5. *p< 0.05. Data were obtained from gepia2.com. (B) Overall survival of basal-like breast cancer patients with high (red) or low (blue) co­expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (D) Disease free survival of pancreatic adenocarcinoma patients with high (red) or low (blue) co-expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (E,F) RNA sequencing data and ROC analysis for the co-expression of SLC3A2 and SLC7A5 from chemoresistant (Non-responder) and chemosensitive (Responder) breast tumours. (E) p = 1,4e-6, Mann-Whitney test. (D) AUG = 0.628; ROC p value = 2.5e-07. Data were generated in ROCplot.com.

    Journal: bioRxiv

    Article Title: Collagen I promotes cancer cell survival via amino acid import and mTORC1 activation

    doi: 10.1101/2025.11.26.690708

    Figure Lengend Snippet: (A,C) RNA sequencing data from basal-Like breast tumours (n=135) and normal breast tissue (n=291) or pancreatic adenocarcinoma tumours (n=179) and normal pancreatic tissue (n=171) for the co-expression of SLC3A2 and SLC7A5. *p< 0.05. Data were obtained from gepia2.com. (B) Overall survival of basal-like breast cancer patients with high (red) or low (blue) co­expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (D) Disease free survival of pancreatic adenocarcinoma patients with high (red) or low (blue) co-expression of SLC3A2 and SLC7A5. Data were obtained from gepia2.com. (E,F) RNA sequencing data and ROC analysis for the co-expression of SLC3A2 and SLC7A5 from chemoresistant (Non-responder) and chemosensitive (Responder) breast tumours. (E) p = 1,4e-6, Mann-Whitney test. (D) AUG = 0.628; ROC p value = 2.5e-07. Data were generated in ROCplot.com.

    Article Snippet: Primary antibodies for Phospho-S6 Ribosomal Protein ser235/236 and LC3A/B were from Cell Signalling; α2 integrin (CD49b)-FITC conjugated and β1 integrin (CD29)-Alexa Fluor 488 conjugated from BioLegend; α2 integrin for Western blotting from BD-bioscience; SLC3A2 (CD98) and SLC7A5 (LAT1) from Proteintech and GAPDH from SANTA CRUZ Biotechnology.

    Techniques: RNA Sequencing, Expressing, MANN-WHITNEY, Generated

    Under Glc starvation, collagen I promoted α2β1 integrin-dependent mTORCI activation in breast and pancreatic cancer cells. Collagen I also increased the membrane levels of the LAT1-4F2hc amino acid transporter heavy chain, SLC3A2 (3A2), and light chain, SLC7A5 (7A5), stimulating amino acid import. This resulted in mTORCI activation and autophagy inhibition, leading to increased survival, proliferation and invasion, in 2D and 3C contexts.

    Journal: bioRxiv

    Article Title: Collagen I promotes cancer cell survival via amino acid import and mTORC1 activation

    doi: 10.1101/2025.11.26.690708

    Figure Lengend Snippet: Under Glc starvation, collagen I promoted α2β1 integrin-dependent mTORCI activation in breast and pancreatic cancer cells. Collagen I also increased the membrane levels of the LAT1-4F2hc amino acid transporter heavy chain, SLC3A2 (3A2), and light chain, SLC7A5 (7A5), stimulating amino acid import. This resulted in mTORCI activation and autophagy inhibition, leading to increased survival, proliferation and invasion, in 2D and 3C contexts.

    Article Snippet: Primary antibodies for Phospho-S6 Ribosomal Protein ser235/236 and LC3A/B were from Cell Signalling; α2 integrin (CD49b)-FITC conjugated and β1 integrin (CD29)-Alexa Fluor 488 conjugated from BioLegend; α2 integrin for Western blotting from BD-bioscience; SLC3A2 (CD98) and SLC7A5 (LAT1) from Proteintech and GAPDH from SANTA CRUZ Biotechnology.

    Techniques: Activation Assay, Membrane, Inhibition

    Figure 6. YAP/TAZ promotes the expression of SLC7A5 to overcome proliferation retardation induced by KRAS inhibitors. (A) Heatmap illustrating the regulation of mTOR-related genes by YAP/TAZ and their dependency for cell survival upon treatment with inhibitors targeting KRAS G12C or MEK. (B) Bar graph presenting the expression of key mTOR-related genes by RT-qPCR in SW1573 cells with or without knockdown of YAP/TAZ upon treatment with AMG510 for 1 day. (C and D) RT-qPCR (C) and immunoblots (D) presenting the expression of SLC7A5 and ERK phosphorylation in KYSE410, SW1573, or H358R cells with or without knockdown of YAP/TAZ, in the presence or absence of 1 day of treatment with 1 μM AMG510. (E and F) RT-qPCR (E) and immunoblots (F) revealing the expression of SLC7A5 in H1373 and MIAPACA2 cells with or without ectopic expression of YAP S127A after treatment with 1 μM AMG510 for 3 days. (G) Dot plots illustrating the expression of SLC7A5 in sensitive and resistant cell lines after different treatment times with 1 μM AMG510. (H) Model elucidating that inhibition of YAP/TAZ enhances the proliferation retardation effect of KRAS G12C inhibitors by downregulating the expression of SLC7A5. Data are presented as mean ± SD (B, C, E, and G). Blots provided together were set up in parallel at the same time (D and F).

    Journal: JCI insight

    Article Title: YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis.

    doi: 10.1172/jci.insight.178535

    Figure Lengend Snippet: Figure 6. YAP/TAZ promotes the expression of SLC7A5 to overcome proliferation retardation induced by KRAS inhibitors. (A) Heatmap illustrating the regulation of mTOR-related genes by YAP/TAZ and their dependency for cell survival upon treatment with inhibitors targeting KRAS G12C or MEK. (B) Bar graph presenting the expression of key mTOR-related genes by RT-qPCR in SW1573 cells with or without knockdown of YAP/TAZ upon treatment with AMG510 for 1 day. (C and D) RT-qPCR (C) and immunoblots (D) presenting the expression of SLC7A5 and ERK phosphorylation in KYSE410, SW1573, or H358R cells with or without knockdown of YAP/TAZ, in the presence or absence of 1 day of treatment with 1 μM AMG510. (E and F) RT-qPCR (E) and immunoblots (F) revealing the expression of SLC7A5 in H1373 and MIAPACA2 cells with or without ectopic expression of YAP S127A after treatment with 1 μM AMG510 for 3 days. (G) Dot plots illustrating the expression of SLC7A5 in sensitive and resistant cell lines after different treatment times with 1 μM AMG510. (H) Model elucidating that inhibition of YAP/TAZ enhances the proliferation retardation effect of KRAS G12C inhibitors by downregulating the expression of SLC7A5. Data are presented as mean ± SD (B, C, E, and G). Blots provided together were set up in parallel at the same time (D and F).

    Article Snippet: Antibodies against YAP (1:1000, sc-101199), GAPDH (1:5000, sc-47724), BCL2L11 (1:500, sc-374358), PUMA (1:500, sc-374223), SLC7A5 (1:1000, sc-374232), and ERK1/2 (1:1000, sc-514302) were from Santa Cruz Biotechnology.

    Techniques: Expressing, Quantitative RT-PCR, Knockdown, Western Blot, Phospho-proteomics, Inhibition

    Figure 10. Model illustrating the roles of YAP/TAZ in developing and maintaining resistance to KRAS inhibitors. KRAS inhibitors (KRASi) can induce upregulation of YAP/TAZ activity, which in turn protects cells from KRAS inhibitor–induced apoptosis by downregulating proapoptotic genes such as BMF, BCL2L11, and PUMA, while also reversing proliferation retardation through activation of the SLC7A5/mTORC1 axis.

    Journal: JCI insight

    Article Title: YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis.

    doi: 10.1172/jci.insight.178535

    Figure Lengend Snippet: Figure 10. Model illustrating the roles of YAP/TAZ in developing and maintaining resistance to KRAS inhibitors. KRAS inhibitors (KRASi) can induce upregulation of YAP/TAZ activity, which in turn protects cells from KRAS inhibitor–induced apoptosis by downregulating proapoptotic genes such as BMF, BCL2L11, and PUMA, while also reversing proliferation retardation through activation of the SLC7A5/mTORC1 axis.

    Article Snippet: Antibodies against YAP (1:1000, sc-101199), GAPDH (1:5000, sc-47724), BCL2L11 (1:500, sc-374358), PUMA (1:500, sc-374223), SLC7A5 (1:1000, sc-374232), and ERK1/2 (1:1000, sc-514302) were from Santa Cruz Biotechnology.

    Techniques: Activity Assay, Activation Assay