Influence of administration methods on the accumulation of ALA‐induced Pp‐IX in mouse tongue tumors

Ogasawara, Toshiyuki; Miyoshi, Norio; Sano, Kazuo; Kitagawa, Yoshimasa; Yamada, Tetsushi; Ogawa, Teiichiro; Miyauchi, Katsuki; Kinoshita, Hidehito

doi:10.1111/j.1601-0825.2006.01216.x

Cited by 9 publications

(7 citation statements)

References 18 publications

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“…Free heme stimulates neutrophils and induces their chemotaxsis via signal pathways characteristic of chemotactic receptors. [27,28] Heme also regulates innate immunity by inducing tumor necrosis factor (TNF) production from dendritic cells (DCs) via myeloid differentiation primary response gene (88) (MyD88), toll-like receptor 4 (TLR4), and CD44 [35].…”

Section: Biological Activity Of Heme and Its Metabolitesmentioning

confidence: 99%

“…There are two ALAS isozymes, ALAS1 and ALAS2, [26] with ALAS1 being expressed in all organs, and ALAS2 expressed only by red blood cells. The half-life of ALAS1 in liver mitochondria is approximately 35 min, [27] and its expression is regulated by the heme regulatory motif (HRM). [28] Therefore, when a high level of heme is present, it will bind to the cysteine-proline (CP) motif of ALAS1, inhibiting the localization of the ALAS1 precursor in the mitochondria.…”

Section: Biosynthesis and Metabolite Of Hemementioning

confidence: 99%

See 1 more Smart Citation

Novel development of 5-aminolevurinic acid (ALA) in cancer diagnoses and therapy

Ishizuka

Abe

Sano

et al. 2011

International Immunopharmacology

228

218

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Section: Biological Activity Of Heme and Its Metabolitesmentioning

confidence: 99%

Section: Biosynthesis and Metabolite Of Hemementioning

confidence: 99%

Novel development of 5-aminolevurinic acid (ALA) in cancer diagnoses and therapy

Ishizuka

Abe

Sano

et al. 2011

International Immunopharmacology

228

218

View full text Add to dashboard Cite

“…The mice were randomly divided into two groups (n = 6/group). After abdominal cavity anesthesia with 1% sodium pentobarbital at a concentration of 500 mg/kg, a total of 1 × 10 7 SCC9 cells overexpressing cyclin G2 or control GFP (NC) cells in 50 µl of PBS was injected into the tongue of the nude mice (20). Mice were housed at room with 40-60% humidity, and with a light cycle of 12 h light and 12 h dark under pathogen-free conditions.…”

Section: Animal Experimentsmentioning

confidence: 99%

Cyclin G2 Inhibits Oral Squamous Cell Carcinoma Growth and Metastasis by Binding to IGFBP3 and Regulating the FAK-SRC-STAT Signaling Pathway

et al. 2020

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The cell cycle protein cyclin G2 is considered a tumor suppressor. However, its regulatory effects and potential mechanisms in oral cancers are not well understood. This study aimed to investigate the effect of cyclin G2 on oral squamous cell carcinoma (OSCC). The data from 80 patients with OSCC were utilized to predict the abnormal expression of cyclin G2. The proliferation and metastasis were determined by a cell counting Kit-8 assay, flow cytometry, a wound-healing assay, and a cell invasion assay. The expression of key proteins and genes associated with the cyclin G2 signaling pathways was determined by western blotting and real-time PCR, respectively. The orthotopic nude mice model was established by a mouth injection of SCC9 cells overexpressing cyclin G2. We showed that the low level of cyclin G2 in OSCC, which is negatively correlated with clinical staging, was a negative prognostic factor for the disease. We also found that cyclin G2 inhibited the proliferation, metastasis, and blocked the cell cycle at G1/S of OSCC cells, suggesting that cyclin G2 has an inhibitory effect in OSCC. Mechanistically, cyclin G2 inhibited the growth and metastasis of OSCC by binding to insulin-like growth factor binding protein 3 (IGFBP3) and regulating the focal adhesion kinase (FAK)-SRC-STAT signal transduction pathway. Cyclin G2 competed with integrin to bind to IGFBP3; the binding between integrin and IGFBP3 was reduced after cyclin G2 overexpression, thereby inhibiting the phosphorylation of FAK and SRC. These results showed that cyclin G2 inhibited the progression of OSCC by interacting with IGFBP3 and that it may be a new target for OSCC treatment.

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“…The mice were randomly divided into two groups (n = 6/ group). After abdominal cavity anesthesia with 1% sodium pentobarbital at a concentration of 500 mg/kg, a total of 1 × 10 7 SCC9 cells overexpressing cyclin G2 or control GFP (NC) cells in 50µl of PBS was injected into the tongue of the nude mice (20). Mice were housed at room with 40-60% humidity, and with a light cycle of 12 hour light and12 hour dark under pathogen-free conditions.…”

Section: Animal Experimentsmentioning

confidence: 99%

Cyclin G2 inhibits oral squamous cell carcinoma growth and metastasis by binding to insulin-like growth factor binding protein 3 and regulating the FAK-SRC-STAT signaling pathway

Wang

Gao

Zhao

et al. 2020

Preprint

View full text Add to dashboard Cite

The cell cycle protein cyclin G2 is considered a tumor suppressor. However, its regulatory effects and potential mechanisms in oral cancers are not well understood. This study aimed to investigate the effect of cyclin G2 on oral squamous cell carcinoma (OSCC). The data from 80 patients with OSCC were utilized to predict the abnormal expression of cyclin G2. The proliferation and metastasis were determined by a cell counting Kit-8 assay, flow cytometry, a wound-healing assay and a cell invasion assay. The expression of key proteins and genes associated with the cyclin G2 signaling pathways was determined by western blotting and real-time PCR, respectively. The orthotopic nude mice model was established by a mouth injection of SCC9 cells overexpressing cyclin G2. We showed that the low level of cyclin G2 in OSCC, which is negatively correlated with clinical staging, was a negative prognostic factor for the disease. We also found that cyclin G2 inhibited the proliferation, metastasis and blocked the cell cycle at G1/S of OSCC cells, suggesting that cyclin G2 has an inhibitory effect in OSCC. Mechanistically, cyclin G2 inhibited the growth and metastasis of OSCC by binding to insulin-like growth factor binding protein 3 (IGFBP3) and regulating the focal adhesion kinase (FAK) -SRC-STAT signal transduction pathway. Cyclin G2 competed with integrin to bind to IGFBP3; the binding between integrin and IGFBP3 was reduced after cyclin G2 overexpression, thereby inhibiting the phosphorylation of FAK and SRC. These results showed that cyclin G2 inhibited the progression of OSCC by interacting with IGFBP3 and that it may be a new target for OSCC treatment.

show abstract

Influence of administration methods on the accumulation of ALA‐induced Pp‐IX in mouse tongue tumors

Abstract: These results suggested that p.o. administration of ALA was the most effective method in ALA-PDT for oral cancer.

Cited by 9 publications

References 18 publications

Novel development of 5-aminolevurinic acid (ALA) in cancer diagnoses and therapy

Novel development of 5-aminolevurinic acid (ALA) in cancer diagnoses and therapy

Cyclin G2 Inhibits Oral Squamous Cell Carcinoma Growth and Metastasis by Binding to IGFBP3 and Regulating the FAK-SRC-STAT Signaling Pathway

Cyclin G2 inhibits oral squamous cell carcinoma growth and metastasis by binding to insulin-like growth factor binding protein 3 and regulating the FAK-SRC-STAT signaling pathway

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