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human malignant melanoma cell line a375 (ATCC)

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ATCC human malignant melanoma cell line a375
Human Malignant Melanoma Cell Line A375, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 5217 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+malignant+melanoma+cell+lines/A-375/pmc13088348-209-33-63
Average 99 stars, based on 5217 article reviews

human malignant melanoma cell line a375 - by Bioz Stars, 2026-09

99/100 stars

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Multiple Displacement Amplification:

Article Title: Design, Synthesis, and Biological Evaluation of Stable Colchicine-Binding Site Tubulin Inhibitors 6-Aryl-2-benzoyl-pyridines as Potential Anticancer Agents.
Article Snippet: We previously reported a potent tubulin inhibitor CH-2-77.. In this study, we optimized the structure of CH-2-77 by blocking metabolically labile sites and synthesized a series of CH-2-77 analogues.. Two compounds, 40a and 60c, preserved the potency while improving the metabolic stability over CH-2-77 by 3to 4-fold (46.8 and 29.4 vs 10.8 min in human microsomes).

Article Title: Method of treating cancer and method of sensitizing cancer cells to the action of chemotherapeutic agents via growth hormone receptor antagonists or knock down
Article Snippet: .. Human malignant melanoma cell lines (part of NCI-60 panel of human cancer cells)—SK-MEL-5 (#HTB-70), SK-MEL-28 (#HTB-72), MALME-3M (#HTB-64), MDA-MB-435S (#HTB-1.29), and not mal human skin fibroblast cells MALME-3 (#HTB-102) cells—were obtained from American Type Culture Collection (ATCC; Manassas, Va.). .. SK-MEL-5 and SK-MEL-28 were grown and maintained in EMEM media (ATCC #30-2003), while MALME-3M and MDA-MB-435S were grown in IMDM (ATCC #30-2005) and RPMI-1640 (ATCC #30-2001) respectively, as indicated by ATCC protocols.

Modification:

Article Title: Long non-coding RNA LINC00520 promotes the proliferation and metastasis of malignant melanoma by inducing the miR-125b-5p/EIF5A2 axis
Article Snippet: TargetScan, miRDB and miRTarBase were used to find the target genes of miRNAs. .. Human malignant melanoma cell lines (A375, A2058, MeWo, CHL-1, SK-MEL-28) were obtained from the American Type Culture Collection (ATCC, USA), and growed in Dulbecco’s modified Eagle’s medium (DMEM; Gibco, USA) with 10% fetal bovine serum (Invitrogen, USA). .. Human epidermal melanocytes (HEMa-LP) was purchased from Invitrogen (USA), and maintained in medium 254 (Cascade Biologics, USA).

Cell Culture:

Article Title: Mitochondria-Targeted Antioxidants MitoQ and MitoTEMPO Do Not Influence BRAF-Driven Malignant Melanoma and KRAS-Driven Lung Cancer Progression in Mice
Article Snippet: The concentrations of amplicons were quantified with Quant-iT PicoGreen dsDNA Assay Kit (P11496, Thermo Fisher, Waltham, MA, USA). .. Human malignant melanoma cell lines (A375 from the American Type Culture Collection; IPC-298 from the German Collection of Microorganisms and Cell Culture) were cultured in DMEM GlutaMAX High Glucose (4.5 g/L, 10569-010) supplemented with 10% fetal bovine serum (10270-106) and 1% penicillin/streptomycin (15070-063). .. Human lung cancer cell lines A549 and H838 were from the American Type Culture Collection and were cultured in DMEM GlutaMAX Low Glucose (1 g/L, 21885-108) supplemented with 10% fetal bovine serum (10270-106) and 1% penicillin/streptomycin (15070-063, Thermo Fisher, Waltham, MA, USA).

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Identification of a circANKRD52 in melanoma cells. (A) The genomic loci of circANKRD52. (B) RT‐qPCR analysis of the expression levels of circANKRD52 and ANKRD52 after treatment with RNase R in A375 and SK‐MEL‐28 cells. (C) RT‐qPCR analysis of the transcriptional stability of circANKRD52 and ANKRD52 after treatment with Actinomycin D in A375 cells. (D) RT‐qPCR analysis of the location of circANKRD52 in A375 and SK‐MEL‐28 cells. (E) FISH analysis of the location of circANKRD52 in A375 and SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CircANKRD52 Augments the Growth and Invasion of Melanoma Cells by Sponging miR ‐141‐3p and Upregulating PRKACB

doi: 10.1111/jcmm.70909

Figure Lengend Snippet: Identification of a circANKRD52 in melanoma cells. (A) The genomic loci of circANKRD52. (B) RT‐qPCR analysis of the expression levels of circANKRD52 and ANKRD52 after treatment with RNase R in A375 and SK‐MEL‐28 cells. (C) RT‐qPCR analysis of the transcriptional stability of circANKRD52 and ANKRD52 after treatment with Actinomycin D in A375 cells. (D) RT‐qPCR analysis of the location of circANKRD52 in A375 and SK‐MEL‐28 cells. (E) FISH analysis of the location of circANKRD52 in A375 and SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. **** p < 0.0001.

Article Snippet: Human malignant melanoma cell lines A375, Hs294T, SK‐MEL‐28 were procured from American Type Culture Collection (ATCC, Manassas, VA, USA) and melanocytes were used as the control cells.

Techniques: Quantitative RT-PCR, Expressing

CircANKRD52 augments proliferation and invasion of melanoma cells. (A) EdU analysis of the cell proliferation activity after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (B) Transwell analysis of the cell invasion capabilities after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (C) Flow cytometry analysis of the cell apoptosis after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (D) Tube formation assay analysis of the angiogenesis ability after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (E) Western blot analysis of the protein levels of VEGF after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CircANKRD52 Augments the Growth and Invasion of Melanoma Cells by Sponging miR ‐141‐3p and Upregulating PRKACB

doi: 10.1111/jcmm.70909

Figure Lengend Snippet: CircANKRD52 augments proliferation and invasion of melanoma cells. (A) EdU analysis of the cell proliferation activity after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (B) Transwell analysis of the cell invasion capabilities after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (C) Flow cytometry analysis of the cell apoptosis after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (D) Tube formation assay analysis of the angiogenesis ability after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (E) Western blot analysis of the protein levels of VEGF after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Techniques: Activity Assay, Transfection, Flow Cytometry, Tube Formation Assay, Western Blot

The circANKRD52 acts as a sponge of miR‐141‐3p in melanoma cells. (A) The RNA pull‐down analysis of the binding between circANKRD52 probe and miRNA in A375 cells. (B) RT‐qPCR analysis of the expression levels of miR‐141‐3p in melanoma and the adjacent normal tissues. (C) Pearson's correlation analysis of the correlation between miR‐141‐3p and circANKRD52 in melanoma tissues. (D) RT‐qPCR analysis of the expression of miR‐141‐3p in melanoma cell lines (A375, Hs294T, and SK‐MEL‐28). (E) The dual luciferase reporter assay indicated the binding between circANKRD52 3′UTR and miR‐141‐3p. (F) RT‐qPCR analysis of the expression of miR‐141‐3p after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (G) RIP analysis of the binding ability between circANKRD52 and Ago2 after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (H) RNA pull‐down assay analysis of the binding between Bio‐circANKRD52 WT and miR‐141‐3p. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CircANKRD52 Augments the Growth and Invasion of Melanoma Cells by Sponging miR ‐141‐3p and Upregulating PRKACB

doi: 10.1111/jcmm.70909

Figure Lengend Snippet: The circANKRD52 acts as a sponge of miR‐141‐3p in melanoma cells. (A) The RNA pull‐down analysis of the binding between circANKRD52 probe and miRNA in A375 cells. (B) RT‐qPCR analysis of the expression levels of miR‐141‐3p in melanoma and the adjacent normal tissues. (C) Pearson's correlation analysis of the correlation between miR‐141‐3p and circANKRD52 in melanoma tissues. (D) RT‐qPCR analysis of the expression of miR‐141‐3p in melanoma cell lines (A375, Hs294T, and SK‐MEL‐28). (E) The dual luciferase reporter assay indicated the binding between circANKRD52 3′UTR and miR‐141‐3p. (F) RT‐qPCR analysis of the expression of miR‐141‐3p after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (G) RIP analysis of the binding ability between circANKRD52 and Ago2 after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (H) RNA pull‐down assay analysis of the binding between Bio‐circANKRD52 WT and miR‐141‐3p. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Techniques: Binding Assay, Quantitative RT-PCR, Expressing, Luciferase, Reporter Assay, Transfection, Pull Down Assay

The miR‐141‐3p reverses circANKRD52‐induced melanoma cell proliferation and invasion. (A) EdU analysis of the cell proliferation activity after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (B) Transwell analysis of the cell invasion capabilities after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (C) Flow cytometry analysis of the cell apoptosis after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (D) Tube formation assay analysis of the angiogenesis ability after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (E) Western blot analysis of the protein levels of VEGF after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CircANKRD52 Augments the Growth and Invasion of Melanoma Cells by Sponging miR ‐141‐3p and Upregulating PRKACB

doi: 10.1111/jcmm.70909

Figure Lengend Snippet: The miR‐141‐3p reverses circANKRD52‐induced melanoma cell proliferation and invasion. (A) EdU analysis of the cell proliferation activity after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (B) Transwell analysis of the cell invasion capabilities after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (C) Flow cytometry analysis of the cell apoptosis after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (D) Tube formation assay analysis of the angiogenesis ability after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. (E) Western blot analysis of the protein levels of VEGF after co‐transfection with oe‐circANKRD52 and miR‐141‐3p mimic into A375 cells or sh‐circANKRD52 and miR‐141‐3p inhibitor into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Techniques: Activity Assay, Cotransfection, Flow Cytometry, Tube Formation Assay, Western Blot

PRKACB is identified as a direct target of miR‐141‐3p in melanoma cells. (A) RT‐qPCR analysis of the PRKACB expression in melanoma and the adjacent normal tissues. (B) Pearson's correlation analysis of the correlations of PRKACB with miR‐141‐3p or circANKRD52 expression in melanoma tissues. (C, D) RT‐qPCR and Western blot analysis of the expression of PRKACB in A375, SK‐MEL‐28, and melanocytes. (E) The dual luciferase reporter assay indicated the binding between miR‐141‐3p and PRKACB 3'UTR. (F) RT‐qPCR analysis of the expression of PRKACB after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (G) RT‐qPCR analysis of the expression of PRKACB after transfection with miR‐141‐3p mimic into A375 cells or miR‐141‐3p inhibitor into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05. # p < 0.05.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CircANKRD52 Augments the Growth and Invasion of Melanoma Cells by Sponging miR ‐141‐3p and Upregulating PRKACB

doi: 10.1111/jcmm.70909

Figure Lengend Snippet: PRKACB is identified as a direct target of miR‐141‐3p in melanoma cells. (A) RT‐qPCR analysis of the PRKACB expression in melanoma and the adjacent normal tissues. (B) Pearson's correlation analysis of the correlations of PRKACB with miR‐141‐3p or circANKRD52 expression in melanoma tissues. (C, D) RT‐qPCR and Western blot analysis of the expression of PRKACB in A375, SK‐MEL‐28, and melanocytes. (E) The dual luciferase reporter assay indicated the binding between miR‐141‐3p and PRKACB 3'UTR. (F) RT‐qPCR analysis of the expression of PRKACB after transfection with oe‐circANKRD52 into A375 cells or sh‐circANKRD52 into SK‐MEL‐28 cells. (G) RT‐qPCR analysis of the expression of PRKACB after transfection with miR‐141‐3p mimic into A375 cells or miR‐141‐3p inhibitor into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05. # p < 0.05.

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Luciferase, Reporter Assay, Binding Assay, Transfection

The circANKRD52/PRKACB axis mediates melanoma cell proliferation and invasion. (A) EdU analysis of the cell proliferation activity after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (B) Transwell analysis of the cell invasion capabilities after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (C) Flow cytometry analysis of the cell apoptosis after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (D) Tube formation assay analysis of the angiogenesis ability after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (E) Western blot analysis of the protein levels of VEGF after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Journal: Journal of Cellular and Molecular Medicine

Article Title: CircANKRD52 Augments the Growth and Invasion of Melanoma Cells by Sponging miR ‐141‐3p and Upregulating PRKACB

doi: 10.1111/jcmm.70909

Figure Lengend Snippet: The circANKRD52/PRKACB axis mediates melanoma cell proliferation and invasion. (A) EdU analysis of the cell proliferation activity after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (B) Transwell analysis of the cell invasion capabilities after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (C) Flow cytometry analysis of the cell apoptosis after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (D) Tube formation assay analysis of the angiogenesis ability after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. (E) Western blot analysis of the protein levels of VEGF after co‐transfection with oe‐circANKRD52 and sh‐PRKACB into A375 cells or sh‐circANKRD52 and oe‐PRKACB into SK‐MEL‐28 cells. Data shown are the mean ± SEM of three experiments. * p < 0.05.

Techniques: Activity Assay, Cotransfection, Flow Cytometry, Tube Formation Assay, Western Blot

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human malignant melanoma cell line a375 (ATCC)

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