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sw 48  (ATCC)


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    Structured Review

    ATCC sw 48
    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and <t>SW-48.</t> ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.
    Sw 48, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 884 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Exceptionally selective voltage-sensor trapping of Na V 1.5 channels by Mg-protoporphyrin impairs cancer cell migration"

    Article Title: Exceptionally selective voltage-sensor trapping of Na V 1.5 channels by Mg-protoporphyrin impairs cancer cell migration

    Journal: Scientific Reports

    doi: 10.1038/s41598-026-37492-0

    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and SW-48. ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.
    Figure Legend Snippet: MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and SW-48. ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.

    Techniques Used: Migration, Expressing, Control, Staining, Transwell Migration Assay, Transmission Assay, Cell Counting, Software, Wound Healing Assay



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    sw 48  (ATCC)
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    ATCC sw 48
    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and <t>SW-48.</t> ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.
    Sw 48, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human crc cell lines sw48
    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and <t>SW-48.</t> ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.
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    ccl  (ATCC)
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    ATCC ccl
    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and <t>SW-48.</t> ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.
    Ccl, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    sw48  (ATCC)
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    ATCC sw48
    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and <t>SW-48.</t> ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.
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    TMEM59L regulates colorectal cancer cells proliferation, migration, and invasion. (A) Western blotting confirmed expression of TMEM59L in different <t>CRC</t> cell lines. (B) Western blotting detects the knockdown of TMEM59L by shRNA and overexpression of TMEM59L by plasmid. (C) Downregulation of TMEM59L suppresses cell proliferation <t>in</t> <t>HCT116</t> cells; overexpression of TMEM59L in <t>SW480</t> promotes cell proliferation. (D) The function of TMEM59L on the migration and invasion ability of CRC cells was detected by Transwell assay. (E) E‐cadherin and Vimentin were evaluated through immunofluorescence staining in TMEM59L knockdown and overexpression CRC cells.
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    ATCC sw48 cell line
    TMEM59L regulates colorectal cancer cells proliferation, migration, and invasion. (A) Western blotting confirmed expression of TMEM59L in different <t>CRC</t> cell lines. (B) Western blotting detects the knockdown of TMEM59L by shRNA and overexpression of TMEM59L by plasmid. (C) Downregulation of TMEM59L suppresses cell proliferation <t>in</t> <t>HCT116</t> cells; overexpression of TMEM59L in <t>SW480</t> promotes cell proliferation. (D) The function of TMEM59L on the migration and invasion ability of CRC cells was detected by Transwell assay. (E) E‐cadherin and Vimentin were evaluated through immunofluorescence staining in TMEM59L knockdown and overexpression CRC cells.
    Sw48 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC cell line sw48
    TMEM59L regulates colorectal cancer cells proliferation, migration, and invasion. (A) Western blotting confirmed expression of TMEM59L in different <t>CRC</t> cell lines. (B) Western blotting detects the knockdown of TMEM59L by shRNA and overexpression of TMEM59L by plasmid. (C) Downregulation of TMEM59L suppresses cell proliferation <t>in</t> <t>HCT116</t> cells; overexpression of TMEM59L in <t>SW480</t> promotes cell proliferation. (D) The function of TMEM59L on the migration and invasion ability of CRC cells was detected by Transwell assay. (E) E‐cadherin and Vimentin were evaluated through immunofluorescence staining in TMEM59L knockdown and overexpression CRC cells.
    Cell Line Sw48, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    ATCC human colon carcinoma cell lines
    TMEM59L regulates colorectal cancer cells proliferation, migration, and invasion. (A) Western blotting confirmed expression of TMEM59L in different <t>CRC</t> cell lines. (B) Western blotting detects the knockdown of TMEM59L by shRNA and overexpression of TMEM59L by plasmid. (C) Downregulation of TMEM59L suppresses cell proliferation <t>in</t> <t>HCT116</t> cells; overexpression of TMEM59L in <t>SW480</t> promotes cell proliferation. (D) The function of TMEM59L on the migration and invasion ability of CRC cells was detected by Transwell assay. (E) E‐cadherin and Vimentin were evaluated through immunofluorescence staining in TMEM59L knockdown and overexpression CRC cells.
    Human Colon Carcinoma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and SW-48. ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.

    Journal: Scientific Reports

    Article Title: Exceptionally selective voltage-sensor trapping of Na V 1.5 channels by Mg-protoporphyrin impairs cancer cell migration

    doi: 10.1038/s41598-026-37492-0

    Figure Lengend Snippet: MgPpIX slows down the migration of cancer cells expressing SCN5A. ( A ) Representative images of MDA-MB-231 cell cultures right after introducing a scratch gap (0 h) and 4 h later. After scratch introduction, the cells were kept in control medium with DMSO (Ctrl) or 100 nM of the indicated MePpIX, dissolved in DMSO. The cells were kept in the dark to prevent phototoxicity induced by the MePpIXs. Continuous black lines indicate the automatically detected scratch borders. Scale bar: 400 µm. ( B ) Mean gap-closure migration of MDA-MB-231 cells (relative to the migration under control conditions, i.e., in the presence of the vehicle DMSO) in the presence of 100 nM of PpIX or the indicated MePpIX variants. C Representative confocal images of DAPI-stained MDA-MB-231 cell nuclei detected on the trans side in a transwell migration assay with an 8 µm pore diameter and a chemoattraction gradient from 0 (insert) to 2% FBS (wells); background in white. The panels on the right show superpositions of the DAPI staining (blue) with transmission images. Cells were kept overnight under control conditions or in the presence of 100 nM of the indicated MePpIX. Images were taken through a 10 × objective with a 3 × zoom factor. Cell counting was performed based on the DAPI staining using ImageJ software. Scale bar: 400 µm. ( D ) Mean number of migrated cells from experiments as shown in ( C ). E Mean migration in a wound-healing assay of MDA-MB-231 cells over 4 h in the presence of the indicated concentrations of MgPpIX, TTX, and PpIX. ( F ) Mean normalized current traces obtained from MDA-MB-231 cells under voltage-clamp conditions with step depolarizations to − 30 mV without (black) and with the application of 100 nM MgPpIX. The currents on the right followed an episode of 250 ms at 40 mV to highlight the reverse use-dependence of these Na V channels. ( G ) Mean relative migration in a wound-healing assay (as in B and E ) but for T-47D cells. ( H ) As in ( G ) but for the colon carcinoma cell lines SW-480 and SW-48. ( I ) Mean current density, based on the peak currents at − 30 mV, for HEK293T cells and the indicated breast cancer (MDA-MB-231, T-47D) and colon carcinoma cells (SW-480, SW-48). Data bars are means ± sem with n in parentheses; in ( B ), ( D ), ( E ), ( G ), and ( H ), the number of independent cell batches is given.

    Article Snippet: The breast cancer cell lines MDA-MB-231 (DSMZ) and T-47D (American Type Culture Collection, ATCC) were cultured in RPMI 1640 medium (Sigma, R7388), while the colorectal cancer cell lines SW-480 (DSMZ) and SW-48 (ATCC) were maintained in DMEM.

    Techniques: Migration, Expressing, Control, Staining, Transwell Migration Assay, Transmission Assay, Cell Counting, Software, Wound Healing Assay

    TMEM59L regulates colorectal cancer cells proliferation, migration, and invasion. (A) Western blotting confirmed expression of TMEM59L in different CRC cell lines. (B) Western blotting detects the knockdown of TMEM59L by shRNA and overexpression of TMEM59L by plasmid. (C) Downregulation of TMEM59L suppresses cell proliferation in HCT116 cells; overexpression of TMEM59L in SW480 promotes cell proliferation. (D) The function of TMEM59L on the migration and invasion ability of CRC cells was detected by Transwell assay. (E) E‐cadherin and Vimentin were evaluated through immunofluorescence staining in TMEM59L knockdown and overexpression CRC cells.

    Journal: Cancer Reports

    Article Title: Transmembrane Protein TMEM59L Modulates 5‐ FU Resistance via PTPRN ‐Mediated DNA Damage Repair in Colorectal Cancer

    doi: 10.1002/cnr2.70448

    Figure Lengend Snippet: TMEM59L regulates colorectal cancer cells proliferation, migration, and invasion. (A) Western blotting confirmed expression of TMEM59L in different CRC cell lines. (B) Western blotting detects the knockdown of TMEM59L by shRNA and overexpression of TMEM59L by plasmid. (C) Downregulation of TMEM59L suppresses cell proliferation in HCT116 cells; overexpression of TMEM59L in SW480 promotes cell proliferation. (D) The function of TMEM59L on the migration and invasion ability of CRC cells was detected by Transwell assay. (E) E‐cadherin and Vimentin were evaluated through immunofluorescence staining in TMEM59L knockdown and overexpression CRC cells.

    Article Snippet: Five human CRC cell lines (NCI‐H716, HCT116, COLO 320DM, SW48, SW480) were sourced from the American Type Culture Collection (ATCC, USA), while a 5‐fluorouracil‐resistant HCT116 subline (HCT116/FU, BNCC342640) was obtained from BNCC (China).

    Techniques: Migration, Western Blot, Expressing, Knockdown, shRNA, Over Expression, Plasmid Preparation, Transwell Assay, Immunofluorescence, Staining

    TMEM59L was elevated in 5‐FU resistance CRC cell lines and reduced 5‐FU sensitivity. (A) The expression of TMEM59L in non‐responder and responder groups treated by 5‐FU ( n = 279 vs. 379, p = 0.0002), oxaliplatin ( n = 173 vs. 265, p = 0.012) and Capecitabine ( n = 62 vs. 47, p = 0.000019), respectively. (B) TMEM59L level in CRC cell lines and corresponding 5‐FU resistant cells was examined by western blot. (C, D) CCK‐8 assays of TMEM59L downregulation and upregulation on sensitivity of HCT116 and SW480 cells to 5‐FU; the half maximal inhibitory concentration (IC50) was calculated using GraphPad software. Data represent the mean ± SD ( n = 3), * p < 0.05 vs. HCT116 group, $ p < 0.05 vs. SW480 group.

    Journal: Cancer Reports

    Article Title: Transmembrane Protein TMEM59L Modulates 5‐ FU Resistance via PTPRN ‐Mediated DNA Damage Repair in Colorectal Cancer

    doi: 10.1002/cnr2.70448

    Figure Lengend Snippet: TMEM59L was elevated in 5‐FU resistance CRC cell lines and reduced 5‐FU sensitivity. (A) The expression of TMEM59L in non‐responder and responder groups treated by 5‐FU ( n = 279 vs. 379, p = 0.0002), oxaliplatin ( n = 173 vs. 265, p = 0.012) and Capecitabine ( n = 62 vs. 47, p = 0.000019), respectively. (B) TMEM59L level in CRC cell lines and corresponding 5‐FU resistant cells was examined by western blot. (C, D) CCK‐8 assays of TMEM59L downregulation and upregulation on sensitivity of HCT116 and SW480 cells to 5‐FU; the half maximal inhibitory concentration (IC50) was calculated using GraphPad software. Data represent the mean ± SD ( n = 3), * p < 0.05 vs. HCT116 group, $ p < 0.05 vs. SW480 group.

    Article Snippet: Five human CRC cell lines (NCI‐H716, HCT116, COLO 320DM, SW48, SW480) were sourced from the American Type Culture Collection (ATCC, USA), while a 5‐fluorouracil‐resistant HCT116 subline (HCT116/FU, BNCC342640) was obtained from BNCC (China).

    Techniques: Expressing, Western Blot, CCK-8 Assay, Concentration Assay, Software

    Silencing of TMEM59L enhanced DNA damage and 5‐FU sensibility in colorectal cancer cells and drug‐resistant CRC cell lines. (A, B) γ‐H2AX foci formation in HCT116 and SW480 cells was detected by immunofluorescence 48 h after treatment with 5‐FU (25 μg/mL). (C) Intracellular ROS levels in HCT116 and SW480 cells treated with 5‐FU for 48 h were detected by reactive oxygen species detection kit. (D) Effect of TMEM59L on apoptosis in CRC cells induced by 5‐FU (25 μg/mL) treatment for 48 h was determined by flow cytometric analysis. (E) Downregulation of TMEM59L reduced colony formation of HCT116/FU and SW480/FU cells.

    Journal: Cancer Reports

    Article Title: Transmembrane Protein TMEM59L Modulates 5‐ FU Resistance via PTPRN ‐Mediated DNA Damage Repair in Colorectal Cancer

    doi: 10.1002/cnr2.70448

    Figure Lengend Snippet: Silencing of TMEM59L enhanced DNA damage and 5‐FU sensibility in colorectal cancer cells and drug‐resistant CRC cell lines. (A, B) γ‐H2AX foci formation in HCT116 and SW480 cells was detected by immunofluorescence 48 h after treatment with 5‐FU (25 μg/mL). (C) Intracellular ROS levels in HCT116 and SW480 cells treated with 5‐FU for 48 h were detected by reactive oxygen species detection kit. (D) Effect of TMEM59L on apoptosis in CRC cells induced by 5‐FU (25 μg/mL) treatment for 48 h was determined by flow cytometric analysis. (E) Downregulation of TMEM59L reduced colony formation of HCT116/FU and SW480/FU cells.

    Article Snippet: Five human CRC cell lines (NCI‐H716, HCT116, COLO 320DM, SW48, SW480) were sourced from the American Type Culture Collection (ATCC, USA), while a 5‐fluorouracil‐resistant HCT116 subline (HCT116/FU, BNCC342640) was obtained from BNCC (China).

    Techniques: Immunofluorescence

    TMEM59L regulated 5‐FU induced DNA damage and ROS through PTPRN. (A) Physical interactions with TMEM59L in GeneMANIA website. (B) Correlation analysis between TMEM59L and PTPRN in COAD from GEPIA database. (C) PTPRN expression in COAD and READ from the TCGA database analyzed by the GEPIA database. (D) Higher PTPRN expression was related to poorer OS in CRC patients from TCGA through Kaplan–Meier Plotter database. (E) PTPRN partially reversed the effect of TMEM59L on 5‐FU induced ROS of HCT116 and SW480 cells. (F) PTPRN partially reversed the effect of TMEM59L on 5‐FU induced DNA damage of HCT116 and SW480 cells.

    Journal: Cancer Reports

    Article Title: Transmembrane Protein TMEM59L Modulates 5‐ FU Resistance via PTPRN ‐Mediated DNA Damage Repair in Colorectal Cancer

    doi: 10.1002/cnr2.70448

    Figure Lengend Snippet: TMEM59L regulated 5‐FU induced DNA damage and ROS through PTPRN. (A) Physical interactions with TMEM59L in GeneMANIA website. (B) Correlation analysis between TMEM59L and PTPRN in COAD from GEPIA database. (C) PTPRN expression in COAD and READ from the TCGA database analyzed by the GEPIA database. (D) Higher PTPRN expression was related to poorer OS in CRC patients from TCGA through Kaplan–Meier Plotter database. (E) PTPRN partially reversed the effect of TMEM59L on 5‐FU induced ROS of HCT116 and SW480 cells. (F) PTPRN partially reversed the effect of TMEM59L on 5‐FU induced DNA damage of HCT116 and SW480 cells.

    Article Snippet: Five human CRC cell lines (NCI‐H716, HCT116, COLO 320DM, SW48, SW480) were sourced from the American Type Culture Collection (ATCC, USA), while a 5‐fluorouracil‐resistant HCT116 subline (HCT116/FU, BNCC342640) was obtained from BNCC (China).

    Techniques: Expressing