Limits...
ANGPTL3 is a novel biomarker as it activates ERK/MAPK pathway in oral cancer.

Koyama T, Ogawara K, Kasamatsu A, Okamoto A, Kasama H, Minakawa Y, Shimada K, Yokoe H, Shiiba M, Tanzawa H, Uzawa K - Cancer Med (2015)

Bottom Line: Significant (P < 0.05) ANGPTL3 upregulation was detected in the cell lines and most primary OSCCs (60%) compared with the normal counterparts.In vitro, cellular growth in ANGPTL3 knockdown cells significantly (P < 0.05) decreased with inactivated extracellular regulated kinase (ERK) and cell-cycle arrest at the G1 phase resulting from upregulation of the cyclin-dependent kinase inhibitors, including p21(Cip1) and p27(Kip1) .The current data indicated that ANGPTL3 may play a role in OSCCs via MAPK signaling cascades, making it a potentially useful diagnostic/therapeutic target for use in patients with OSCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

No MeSH data available.


Related in: MedlinePlus

Evaluation of ANGPTL3 expression in OSCC-derived cell lines. (A) Quantification of ANGPTL3 mRNA expression in OSCC-derived cell lines by qRT-PCR analysis. Significant (*P < 0.05, Mann–Whitney U-test) upregulation of ANGPTL3 mRNA is seen in seven OSCC-derived cell lines compared with the HNOKs. Data are expressed as the mean ± SEM of triplicate results. (B) Immunoblotting analysis of ANGPTL3 protein in the OSCC-derived cell lines and HNOKs. ANGPTL3 protein expression is upregulated in the OSCC-derived cell lines compared with the HNOKs. Densitometric ANGPTL3 protein data are normalized to GAPDH protein levels. The values are expressed as a percentage of the HNOKs (P < 0.05, Mann–Whitney U-test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4430268&req=5

fig01: Evaluation of ANGPTL3 expression in OSCC-derived cell lines. (A) Quantification of ANGPTL3 mRNA expression in OSCC-derived cell lines by qRT-PCR analysis. Significant (*P < 0.05, Mann–Whitney U-test) upregulation of ANGPTL3 mRNA is seen in seven OSCC-derived cell lines compared with the HNOKs. Data are expressed as the mean ± SEM of triplicate results. (B) Immunoblotting analysis of ANGPTL3 protein in the OSCC-derived cell lines and HNOKs. ANGPTL3 protein expression is upregulated in the OSCC-derived cell lines compared with the HNOKs. Densitometric ANGPTL3 protein data are normalized to GAPDH protein levels. The values are expressed as a percentage of the HNOKs (P < 0.05, Mann–Whitney U-test).

Mentions: To investigate the expression status of ANGPTL3, we performed qRT-PCR and immunoblotting analyses using eight OSCC-derived cell lines (Ho-1-N-1, Ho-1-u-1, HSC-2, HSC-3, HSC-4, Sa3, KOSC-2, and Ca9-22) and HNOKs. ANGPTL3 mRNA was upregulated significantly (P < 0.05) in all OSCC-derived cell lines compared with the HNOKs (Fig.1A). Representative results of immunoblotting analysis are shown in Figure1B. The ANGPTL3 protein expression decreased significantly (P < 0.05) in all OSCC-derived cell lines compared with the HNOKs.


ANGPTL3 is a novel biomarker as it activates ERK/MAPK pathway in oral cancer.

Koyama T, Ogawara K, Kasamatsu A, Okamoto A, Kasama H, Minakawa Y, Shimada K, Yokoe H, Shiiba M, Tanzawa H, Uzawa K - Cancer Med (2015)

Evaluation of ANGPTL3 expression in OSCC-derived cell lines. (A) Quantification of ANGPTL3 mRNA expression in OSCC-derived cell lines by qRT-PCR analysis. Significant (*P < 0.05, Mann–Whitney U-test) upregulation of ANGPTL3 mRNA is seen in seven OSCC-derived cell lines compared with the HNOKs. Data are expressed as the mean ± SEM of triplicate results. (B) Immunoblotting analysis of ANGPTL3 protein in the OSCC-derived cell lines and HNOKs. ANGPTL3 protein expression is upregulated in the OSCC-derived cell lines compared with the HNOKs. Densitometric ANGPTL3 protein data are normalized to GAPDH protein levels. The values are expressed as a percentage of the HNOKs (P < 0.05, Mann–Whitney U-test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4430268&req=5

fig01: Evaluation of ANGPTL3 expression in OSCC-derived cell lines. (A) Quantification of ANGPTL3 mRNA expression in OSCC-derived cell lines by qRT-PCR analysis. Significant (*P < 0.05, Mann–Whitney U-test) upregulation of ANGPTL3 mRNA is seen in seven OSCC-derived cell lines compared with the HNOKs. Data are expressed as the mean ± SEM of triplicate results. (B) Immunoblotting analysis of ANGPTL3 protein in the OSCC-derived cell lines and HNOKs. ANGPTL3 protein expression is upregulated in the OSCC-derived cell lines compared with the HNOKs. Densitometric ANGPTL3 protein data are normalized to GAPDH protein levels. The values are expressed as a percentage of the HNOKs (P < 0.05, Mann–Whitney U-test).
Mentions: To investigate the expression status of ANGPTL3, we performed qRT-PCR and immunoblotting analyses using eight OSCC-derived cell lines (Ho-1-N-1, Ho-1-u-1, HSC-2, HSC-3, HSC-4, Sa3, KOSC-2, and Ca9-22) and HNOKs. ANGPTL3 mRNA was upregulated significantly (P < 0.05) in all OSCC-derived cell lines compared with the HNOKs (Fig.1A). Representative results of immunoblotting analysis are shown in Figure1B. The ANGPTL3 protein expression decreased significantly (P < 0.05) in all OSCC-derived cell lines compared with the HNOKs.

Bottom Line: Significant (P < 0.05) ANGPTL3 upregulation was detected in the cell lines and most primary OSCCs (60%) compared with the normal counterparts.In vitro, cellular growth in ANGPTL3 knockdown cells significantly (P < 0.05) decreased with inactivated extracellular regulated kinase (ERK) and cell-cycle arrest at the G1 phase resulting from upregulation of the cyclin-dependent kinase inhibitors, including p21(Cip1) and p27(Kip1) .The current data indicated that ANGPTL3 may play a role in OSCCs via MAPK signaling cascades, making it a potentially useful diagnostic/therapeutic target for use in patients with OSCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral Science, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

No MeSH data available.


Related in: MedlinePlus