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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

ANGPTL3 promotes tumoral growth in vivo. (A) ShANGPTL3- and shMock-transfected cells (HSC-3 and Sa3) were injected subcutaneously into the backs of female nude mice (n = 3). Tumoral growth in the shANGTPL3-injected mice is inhibited significantly (*P < 0.05; Mann–Whitney U-test) compared to the shMock-injected mice. (B) IHC of the xenografted tumors clearly shows more decreased immunostaining for ANGPTL3 and pERK in the xenografted tumors from shANGPTL3 transfectants than shMock transfectants. H&E staining confirmed the presence of tumoral cells. Original magnification, ×400. Scale bars, 50 μm.
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fig04: ANGPTL3 promotes tumoral growth in vivo. (A) ShANGPTL3- and shMock-transfected cells (HSC-3 and Sa3) were injected subcutaneously into the backs of female nude mice (n = 3). Tumoral growth in the shANGTPL3-injected mice is inhibited significantly (*P < 0.05; Mann–Whitney U-test) compared to the shMock-injected mice. (B) IHC of the xenografted tumors clearly shows more decreased immunostaining for ANGPTL3 and pERK in the xenografted tumors from shANGPTL3 transfectants than shMock transfectants. H&E staining confirmed the presence of tumoral cells. Original magnification, ×400. Scale bars, 50 μm.

Mentions: We assessed the effect of ANGPTL3 on tumoral growth in vivo by evaluating to target tumor xenografts in nude mice. shANGPTL3- and shMock-transfected cells of two cell lines, HSC-3 and Sa3 were injected subcutaneously into the backs of female nude mice, respectively (three mice in each group). According to our in vitro findings, the mean tumoral volume of the shANGPTL3-transfected cells was significantly (P < 0.05) smaller than that of the shMock-transfected cells (Fig.4A). ANGPTL3 IHC of tumoral sections showed that ANGPTL3 knockdown was maintained in vivo. Xenografted tumors of ANGPTL3 knockdown cells showed a significant decrease in the pERK and Ki-67 levels (Fig.4B and Fig. S1B). However, the ERK levels were unchanged. These study provided that ANGPTL3 promotes tumoral growth by the ERK pathway in nude mice.


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)

ANGPTL3 promotes tumoral growth in vivo. (A) ShANGPTL3- and shMock-transfected cells (HSC-3 and Sa3) were injected subcutaneously into the backs of female nude mice (n = 3). Tumoral growth in the shANGTPL3-injected mice is inhibited significantly (*P < 0.05; Mann–Whitney U-test) compared to the shMock-injected mice. (B) IHC of the xenografted tumors clearly shows more decreased immunostaining for ANGPTL3 and pERK in the xenografted tumors from shANGPTL3 transfectants than shMock transfectants. H&E staining confirmed the presence of tumoral cells. Original magnification, ×400. Scale bars, 50 μm.
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Related In: Results  -  Collection

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fig04: ANGPTL3 promotes tumoral growth in vivo. (A) ShANGPTL3- and shMock-transfected cells (HSC-3 and Sa3) were injected subcutaneously into the backs of female nude mice (n = 3). Tumoral growth in the shANGTPL3-injected mice is inhibited significantly (*P < 0.05; Mann–Whitney U-test) compared to the shMock-injected mice. (B) IHC of the xenografted tumors clearly shows more decreased immunostaining for ANGPTL3 and pERK in the xenografted tumors from shANGPTL3 transfectants than shMock transfectants. H&E staining confirmed the presence of tumoral cells. Original magnification, ×400. Scale bars, 50 μm.
Mentions: We assessed the effect of ANGPTL3 on tumoral growth in vivo by evaluating to target tumor xenografts in nude mice. shANGPTL3- and shMock-transfected cells of two cell lines, HSC-3 and Sa3 were injected subcutaneously into the backs of female nude mice, respectively (three mice in each group). According to our in vitro findings, the mean tumoral volume of the shANGPTL3-transfected cells was significantly (P < 0.05) smaller than that of the shMock-transfected cells (Fig.4A). ANGPTL3 IHC of tumoral sections showed that ANGPTL3 knockdown was maintained in vivo. Xenografted tumors of ANGPTL3 knockdown cells showed a significant decrease in the pERK and Ki-67 levels (Fig.4B and Fig. S1B). However, the ERK levels were unchanged. These study provided that ANGPTL3 promotes tumoral growth by the ERK pathway in nude mice.

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