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ATCC human pancreatic cancer cell lines panc 01

Human Pancreatic Cancer Cell Lines Panc 01, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7820 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human pancreatic cancer cell lines panc 01 - by Bioz Stars, 2026-05

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1) Product Images from "The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration"

Article Title: The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration

Journal: Scientific Reports

doi: 10.1038/s41598-026-50740-7

Figure Legend Snippet: Knockdown of C16orf87 causes minor changes in the host cell protein profile. ( A ) Alignment of human ( Homo sapiens , UniProtKB accession number Q6PH81 ), mouse ( Mus musculus , UniProtKB accession number Q9CR55 ), and zebrafish ( Danio rerio , UniProtKB accession number Q6DGQ4 ) C16orf87 amino acid sequences. Alignment mismatches are indicated in gray boxes. The underlined sequence represents a possible minimal Akt/PKB kinase consensus recognition motif. A Ser91(S91) phosphorylation site is marked with an asterisk. ( B ) Per-residue confidence (pLDDT) coloring of the top-ranked predicted model of C16orf87. In the inset, the predicted zinc-ribbon domain is shown with the zinc-interacting cysteines (Cys16, Cys19, Cys30, and Cys32) indicated around the zinc ion (Zn 2+ ). The position of the phosphorylated serine (Ser91), a putative alpha-helix between amino acid residues Ser-107 and Ala-126, and the confidently predicted C-terminal alpha-helix between amino acid residues Asp-130 and Ile-153 are also highlighted. The ipTM and pTM values are annotated. N, N-terminus; C, C-terminus. Figure was rendered using ChimeraX (version 1.8, https://www.rbvi.ucsf.edu/chimerax ) ( C ) Western blot (WB) analysis of C16orf87 siRNA (siC16) knockdown in Panc-01, MiaPaCa-2, and C2C12 cell lines. A non-specific, scrambled siRNA (siScr) was used as a control; the WB membrane was probed with the antibodies against C16orf87 and actin. MS-based proteomics analysis of siRNA-treated C2C12 ( D ), MiaPaCa-2 ( E ), and Panc-01 ( F ) cells. Data points corresponding to histones are colored in pink, and statistically significant ( P < 0.05, fold-change > 1) proteins are colored in yellow (mouse cell line C2C12) and green (human cell lines, Panc-01 and MiaPaCa-2).

Techniques Used: Knockdown, Sequencing, Phospho-proteomics, Residue, Western Blot, Control, Membrane

CRISPR-Cas9 knockout of C16orf87 does not affect Panc-01 cell viability. ( A ) Whole-cell lysates of Panc-01 KO and Panc-01 WT cells were analyzed by western blot (WB), and proteins were detected with the antibodies against C16orf87 and actin. An asterisk indicates the migration of the C16orf87 protein. Mw; molecular weight marker. ( B ) MS-based proteomics analysis of Panc-01 KO and Panc-01 WT cell lysates (FDR ≤ 0.05, n = 3). Data points representing histones and proteins of interest are highlighted in red. ( C ) Panc-01 KO and Panc-01 WT cell viability was analyzed by FACS after AnnexinV-FITC (AnnV) and DRAQ7 (Dq7) staining. ( D ) Panc-01 KO and Panc-01 WT cell proliferation was analyzed by FACS after EdU-A647 incorporation into cells. ( E ) Quantification of the FACS analysis ( P < 0.01 (**)).

Figure Legend Snippet: CRISPR-Cas9 knockout of C16orf87 does not affect Panc-01 cell viability. ( A ) Whole-cell lysates of Panc-01 KO and Panc-01 WT cells were analyzed by western blot (WB), and proteins were detected with the antibodies against C16orf87 and actin. An asterisk indicates the migration of the C16orf87 protein. Mw; molecular weight marker. ( B ) MS-based proteomics analysis of Panc-01 KO and Panc-01 WT cell lysates (FDR ≤ 0.05, n = 3). Data points representing histones and proteins of interest are highlighted in red. ( C ) Panc-01 KO and Panc-01 WT cell viability was analyzed by FACS after AnnexinV-FITC (AnnV) and DRAQ7 (Dq7) staining. ( D ) Panc-01 KO and Panc-01 WT cell proliferation was analyzed by FACS after EdU-A647 incorporation into cells. ( E ) Quantification of the FACS analysis ( P < 0.01 (**)).

Techniques Used: CRISPR, Knock-Out, Western Blot, Migration, Molecular Weight, Marker, Staining

CRISPR-Cas9 knockout of C16orf87 reduces Panc-01 cell migration. ( A ) Microscopy images of the in vitro scratch assay in Panc-01 KO and Panc-01 WT cells. Images were taken at 0, 6, 12, and 24 h after scratches were applied. ( B ) The cell migration rate was calculated based on the extent of cell coverage within the scratched area ( P < 0.05 (*) and P < 0.01 (**)).

Figure Legend Snippet: CRISPR-Cas9 knockout of C16orf87 reduces Panc-01 cell migration. ( A ) Microscopy images of the in vitro scratch assay in Panc-01 KO and Panc-01 WT cells. Images were taken at 0, 6, 12, and 24 h after scratches were applied. ( B ) The cell migration rate was calculated based on the extent of cell coverage within the scratched area ( P < 0.05 (*) and P < 0.01 (**)).

Techniques Used: CRISPR, Knock-Out, Migration, Microscopy, In Vitro, Wound Healing Assay

C16orf87 partially mediates HDAC1 and MIER1 protein interactions. ( A ) C16orf87 interacts with the HDAC and MIER proteins. Volcano plot of the IP-MS experiment showing identified proteins interacting with the Flag-C16orf87 protein in HeLa cells. An adjusted P -value cut-off of 0.05 and a log2 fold change cut-off of 2 were used. Data are shown from a biological triplicate experiment. ( B ) Lack of C16orf87 does not change HDAC and MIER protein accumulation. Soluble Panc-01 WT (WT) and Panc-01 KO (KO) whole-cell lysates were analyzed by WB with the indicated antibodies. ( C ) C16orf87 partially mediates HDAC1 and MIER1 interaction. Co-immunoprecipitation of Flag-HDAC1 from siRNA (siC16 and siScr) and pcDNA3-Flag-HDAC1-transfected HeLa cells. Isolated proteins were analyzed by WB with the indicated antibodies. An arrowhead indicates the migration of the MIER1 protein isoforms, whereas an asterisk indicates the migration of the C16orf87 isoforms. ( D ) HDAC1 interacts weakly with C16orf87 in vitro. GST (as a control) and GST-HDAC1 pull-down with bacterially purified 8 × His-tagged C16orf87(Wt, 5 × C > A, 1–130, and 5 × C > A/1–130) proteins. An asterisk indicates a degradation product/partially translated GST-HDAC1. Proteins were detected with the anti-His and anti-GST antibodies.

Figure Legend Snippet: C16orf87 partially mediates HDAC1 and MIER1 protein interactions. ( A ) C16orf87 interacts with the HDAC and MIER proteins. Volcano plot of the IP-MS experiment showing identified proteins interacting with the Flag-C16orf87 protein in HeLa cells. An adjusted P -value cut-off of 0.05 and a log2 fold change cut-off of 2 were used. Data are shown from a biological triplicate experiment. ( B ) Lack of C16orf87 does not change HDAC and MIER protein accumulation. Soluble Panc-01 WT (WT) and Panc-01 KO (KO) whole-cell lysates were analyzed by WB with the indicated antibodies. ( C ) C16orf87 partially mediates HDAC1 and MIER1 interaction. Co-immunoprecipitation of Flag-HDAC1 from siRNA (siC16 and siScr) and pcDNA3-Flag-HDAC1-transfected HeLa cells. Isolated proteins were analyzed by WB with the indicated antibodies. An arrowhead indicates the migration of the MIER1 protein isoforms, whereas an asterisk indicates the migration of the C16orf87 isoforms. ( D ) HDAC1 interacts weakly with C16orf87 in vitro. GST (as a control) and GST-HDAC1 pull-down with bacterially purified 8 × His-tagged C16orf87(Wt, 5 × C > A, 1–130, and 5 × C > A/1–130) proteins. An asterisk indicates a degradation product/partially translated GST-HDAC1. Proteins were detected with the anti-His and anti-GST antibodies.

Techniques Used: Protein-Protein interactions, Immunoprecipitation, Transfection, Isolation, Migration, In Vitro, Control, Purification

Lack of C16orf87 alters chromatin accessibility. ( A ) Distribution of the more accessible chromatin genomic features identified by ATAC-seq in Panc-01 WT and Panc-01 KO cells. The X-axis shows values in percentage. Gene locus diagrams showing genomic regions near the WWOX ( B ) and NCOA7-HINT3 ( C ) genes, with peaks representing ATAC-seq reads indicating chromatin accessibility. Data were aligned to available tracks (ChIP-Atlas) of HDAC1 , HDAC2 , MIER1 , MIER2 , MIER3 , and H3K27ac markers. Panc-01 WT and Panc-01 KO peaks are shown in blue and green, respectively, and significant differences (FDR threshold: 0.05) in read quantities (peaks), observed in genomic intervals, are shown in red bars on the third track (top to bottom). WWOX represents one of the genes with a higher peak on the Panc-01 WT compared to Panc-01 KO . NCOA7-HINT3 represents one of the genes with higher peaks on the Panc-01 KO . ( D ) qRT-PCR analysis of the NCOA7 , HINT3 , WWOX , and C16orf87 mRNA expression. Relative mRNA expression in Panc-01 WT and Panc-01 KO cells after normalization to 18S rRNA and considering mRNA levels in Panc-01 WT cells as 1.

Figure Legend Snippet: Lack of C16orf87 alters chromatin accessibility. ( A ) Distribution of the more accessible chromatin genomic features identified by ATAC-seq in Panc-01 WT and Panc-01 KO cells. The X-axis shows values in percentage. Gene locus diagrams showing genomic regions near the WWOX ( B ) and NCOA7-HINT3 ( C ) genes, with peaks representing ATAC-seq reads indicating chromatin accessibility. Data were aligned to available tracks (ChIP-Atlas) of HDAC1 , HDAC2 , MIER1 , MIER2 , MIER3 , and H3K27ac markers. Panc-01 WT and Panc-01 KO peaks are shown in blue and green, respectively, and significant differences (FDR threshold: 0.05) in read quantities (peaks), observed in genomic intervals, are shown in red bars on the third track (top to bottom). WWOX represents one of the genes with a higher peak on the Panc-01 WT compared to Panc-01 KO . NCOA7-HINT3 represents one of the genes with higher peaks on the Panc-01 KO . ( D ) qRT-PCR analysis of the NCOA7 , HINT3 , WWOX , and C16orf87 mRNA expression. Relative mRNA expression in Panc-01 WT and Panc-01 KO cells after normalization to 18S rRNA and considering mRNA levels in Panc-01 WT cells as 1.

Techniques Used: Quantitative RT-PCR, Expressing

Image Search Results

Journal: Scientific Reports

Article Title: The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration

doi: 10.1038/s41598-026-50740-7

Figure Lengend Snippet: Knockdown of C16orf87 causes minor changes in the host cell protein profile. ( A ) Alignment of human ( Homo sapiens , UniProtKB accession number Q6PH81 ), mouse ( Mus musculus , UniProtKB accession number Q9CR55 ), and zebrafish ( Danio rerio , UniProtKB accession number Q6DGQ4 ) C16orf87 amino acid sequences. Alignment mismatches are indicated in gray boxes. The underlined sequence represents a possible minimal Akt/PKB kinase consensus recognition motif. A Ser91(S91) phosphorylation site is marked with an asterisk. ( B ) Per-residue confidence (pLDDT) coloring of the top-ranked predicted model of C16orf87. In the inset, the predicted zinc-ribbon domain is shown with the zinc-interacting cysteines (Cys16, Cys19, Cys30, and Cys32) indicated around the zinc ion (Zn 2+ ). The position of the phosphorylated serine (Ser91), a putative alpha-helix between amino acid residues Ser-107 and Ala-126, and the confidently predicted C-terminal alpha-helix between amino acid residues Asp-130 and Ile-153 are also highlighted. The ipTM and pTM values are annotated. N, N-terminus; C, C-terminus. Figure was rendered using ChimeraX (version 1.8, https://www.rbvi.ucsf.edu/chimerax ) ( C ) Western blot (WB) analysis of C16orf87 siRNA (siC16) knockdown in Panc-01, MiaPaCa-2, and C2C12 cell lines. A non-specific, scrambled siRNA (siScr) was used as a control; the WB membrane was probed with the antibodies against C16orf87 and actin. MS-based proteomics analysis of siRNA-treated C2C12 ( D ), MiaPaCa-2 ( E ), and Panc-01 ( F ) cells. Data points corresponding to histones are colored in pink, and statistically significant ( P < 0.05, fold-change > 1) proteins are colored in yellow (mouse cell line C2C12) and green (human cell lines, Panc-01 and MiaPaCa-2).

Article Snippet: Human pancreatic cancer cell lines Panc-01 (ATCC, CRL-1469) and MiaPaCa-2 (ATCC, CRL-1420), mouse skeletal muscle cell line C2C12 (ATCC, CRL-1772), and human cervical cancer cell line HeLa S3 (ATCC, CCL-2.2) were used in this study.

Techniques: Knockdown, Sequencing, Phospho-proteomics, Residue, Western Blot, Control, Membrane

Journal: Scientific Reports

Article Title: The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration

doi: 10.1038/s41598-026-50740-7

Figure Lengend Snippet: CRISPR-Cas9 knockout of C16orf87 does not affect Panc-01 cell viability. ( A ) Whole-cell lysates of Panc-01 KO and Panc-01 WT cells were analyzed by western blot (WB), and proteins were detected with the antibodies against C16orf87 and actin. An asterisk indicates the migration of the C16orf87 protein. Mw; molecular weight marker. ( B ) MS-based proteomics analysis of Panc-01 KO and Panc-01 WT cell lysates (FDR ≤ 0.05, n = 3). Data points representing histones and proteins of interest are highlighted in red. ( C ) Panc-01 KO and Panc-01 WT cell viability was analyzed by FACS after AnnexinV-FITC (AnnV) and DRAQ7 (Dq7) staining. ( D ) Panc-01 KO and Panc-01 WT cell proliferation was analyzed by FACS after EdU-A647 incorporation into cells. ( E ) Quantification of the FACS analysis ( P < 0.01 (**)).

Techniques: CRISPR, Knock-Out, Western Blot, Migration, Molecular Weight, Marker, Staining

Journal: Scientific Reports

Article Title: The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration

doi: 10.1038/s41598-026-50740-7

Figure Lengend Snippet: CRISPR-Cas9 knockout of C16orf87 reduces Panc-01 cell migration. ( A ) Microscopy images of the in vitro scratch assay in Panc-01 KO and Panc-01 WT cells. Images were taken at 0, 6, 12, and 24 h after scratches were applied. ( B ) The cell migration rate was calculated based on the extent of cell coverage within the scratched area ( P < 0.05 (*) and P < 0.01 (**)).

Techniques: CRISPR, Knock-Out, Migration, Microscopy, In Vitro, Wound Healing Assay

Journal: Scientific Reports

Article Title: The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration

doi: 10.1038/s41598-026-50740-7

Figure Lengend Snippet: C16orf87 partially mediates HDAC1 and MIER1 protein interactions. ( A ) C16orf87 interacts with the HDAC and MIER proteins. Volcano plot of the IP-MS experiment showing identified proteins interacting with the Flag-C16orf87 protein in HeLa cells. An adjusted P -value cut-off of 0.05 and a log2 fold change cut-off of 2 were used. Data are shown from a biological triplicate experiment. ( B ) Lack of C16orf87 does not change HDAC and MIER protein accumulation. Soluble Panc-01 WT (WT) and Panc-01 KO (KO) whole-cell lysates were analyzed by WB with the indicated antibodies. ( C ) C16orf87 partially mediates HDAC1 and MIER1 interaction. Co-immunoprecipitation of Flag-HDAC1 from siRNA (siC16 and siScr) and pcDNA3-Flag-HDAC1-transfected HeLa cells. Isolated proteins were analyzed by WB with the indicated antibodies. An arrowhead indicates the migration of the MIER1 protein isoforms, whereas an asterisk indicates the migration of the C16orf87 isoforms. ( D ) HDAC1 interacts weakly with C16orf87 in vitro. GST (as a control) and GST-HDAC1 pull-down with bacterially purified 8 × His-tagged C16orf87(Wt, 5 × C > A, 1–130, and 5 × C > A/1–130) proteins. An asterisk indicates a degradation product/partially translated GST-HDAC1. Proteins were detected with the anti-His and anti-GST antibodies.

Techniques: Protein-Protein interactions, Immunoprecipitation, Transfection, Isolation, Migration, In Vitro, Control, Purification

Journal: Scientific Reports

Article Title: The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration

doi: 10.1038/s41598-026-50740-7

Figure Lengend Snippet: Lack of C16orf87 alters chromatin accessibility. ( A ) Distribution of the more accessible chromatin genomic features identified by ATAC-seq in Panc-01 WT and Panc-01 KO cells. The X-axis shows values in percentage. Gene locus diagrams showing genomic regions near the WWOX ( B ) and NCOA7-HINT3 ( C ) genes, with peaks representing ATAC-seq reads indicating chromatin accessibility. Data were aligned to available tracks (ChIP-Atlas) of HDAC1 , HDAC2 , MIER1 , MIER2 , MIER3 , and H3K27ac markers. Panc-01 WT and Panc-01 KO peaks are shown in blue and green, respectively, and significant differences (FDR threshold: 0.05) in read quantities (peaks), observed in genomic intervals, are shown in red bars on the third track (top to bottom). WWOX represents one of the genes with a higher peak on the Panc-01 WT compared to Panc-01 KO . NCOA7-HINT3 represents one of the genes with higher peaks on the Panc-01 KO . ( D ) qRT-PCR analysis of the NCOA7 , HINT3 , WWOX , and C16orf87 mRNA expression. Relative mRNA expression in Panc-01 WT and Panc-01 KO cells after normalization to 18S rRNA and considering mRNA levels in Panc-01 WT cells as 1.

Techniques: Quantitative RT-PCR, Expressing

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1) Product Images from "The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration"

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