5-aminolevulinic acid induce apoptosis via NF-κB/JNK pathway in human oral cancer Ca9-22 cells

Chen, Hsin‐Ming; Liu, Cheing-Meei; Yang, Hui‐Fang; Chou, Hong‐Nong; Chiang, Chun-Pin; Kuo, Mark Yen‐Ping

doi:10.1111/j.1600-0714.2010.00973.x

Cited by 37 publications

(26 citation statements)

References 32 publications

(50 reference statements)

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“…5-ALA induces effective accumulation of PS Pp IX in tumor cell and has high clearance rate in vivo without phototoxicities. Some studies have demonstrated that 5-ALA/PDT can effectively inhibit the growth of cancer cells in vitro (Peng et al, 1997;He et al, 2008;Chen et al, 2011a;Chen et al, 2011b;Gui et al, 2012). The same PDT result in our study also demonstrated that 5-ALA/PDT induced cytotoxicity depending on PS concentrations.…”

Section: Discussionsupporting

confidence: 78%

Synergistic Anticancer Activity of 5-Aminolevulinic Acid Photodynamic Therapy in Combination with Low-dose Cisplatin on Hela Cells

Wei¹,

Ma²,

Liu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 78%

Synergistic Anticancer Activity of 5-Aminolevulinic Acid Photodynamic Therapy in Combination with Low-dose Cisplatin on Hela Cells

Wei¹,

Ma²,

Liu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…The activation of NF-κB induced by PDT was first found by Ryter et al in their study on the Photofrinmediated PDT treatment of leukemia in 1993 [21]. Researchers have subsequently found this phenomenon in PDT mediated by other photosensitizers, such as 5-ALA and zinc phthalocyanine [22][23][24]. Activated NF-κB induced cell apoptosis through the JNK pathway in a study of Ca9-22 oral cancer cells treated with 5-ALA-PDT [22].…”

Section: Discussionmentioning

confidence: 90%

“…Researchers have subsequently found this phenomenon in PDT mediated by other photosensitizers, such as 5-ALA and zinc phthalocyanine [22][23][24]. Activated NF-κB induced cell apoptosis through the JNK pathway in a study of Ca9-22 oral cancer cells treated with 5-ALA-PDT [22]. Broekgaarden et al found that siRNA knockdown of NF-κB increased survival signaling in murine breast carcinoma (EMT-6) cells and exacerbated the inflammatory response in murine RAW 264.7 macrophages.…”

Section: Discussionmentioning

confidence: 99%

Dihydroartemisinin Increases the Sensitivity of Photodynamic Therapy Via NF-κB/HIF-1α/VEGF Pathway in Esophageal Cancer Cell in vitro and in vivo

Sui

Jiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Although photodynamic therapy (PDT) can relieve esophageal obstruction and prolong survival time of patients with esophageal cancer, it can induce nuclear factor-kappa B (NF-κB) activation in many cancers, which plays a negative role in PDT. Dihydroartemisinin (DHA), the most potent artemisinin derivative, can enhance the effect of PDT on esophageal cancer cells. However, the mechanism is still unclear. Methods: We generated stable cell lines expressing the super-repressor form of the NF-κB inhibitor IκBα and cell lines with lentivirus vector-mediated silencing of the HIF-1α gene. Esophageal xenograft tumors were created by subcutaneous injection of Eca109 cells into BALB/c nude mice. Four treatment groups were analyzed: a control group, photosensitizer alone group, light alone group, and PDT group. NF-κB expression was detected by an electrophoretic mobility shift assay, hypoxia-inducible factor α (HIF-1α) and vascular endothelial growth factor (VEGF) by real-time PCR, NF-κB, HIF-1α, and VEGF protein by western blot, and Ki-67, HIF-1α, VEGF, and NF-κB protein by immunohistochemistry. Results: PDT increased NF-κB activity and the gene expression of HIF-1α and VEGF in vitro and in vivo. In contrast, the DHA groups, particularly the combined DHA and PDT treatment group, abolished the effect. The combined treatment significantly inhibited tumor growth in vitro and in vivo. NF-κB activity and HIF-1α expression were also reduced in the stable IκBα expression group, whereas the former showed no change in HIF-1α-silenced cells. Conclusion: DHA might increase the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway.

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“…Previous studies examined the role of JNK in mediating the apoptotic effect of several pharmacological agents or anticancer drugs in HNSCC cell lines, including N-(4-hydroxyphenyl) retinamide (4HPR), pepsin-digested bovine lactoferrin, 5-aminolevulinic acid, MLN4924, 6-(N, N -dimethylamino)-2-(naphthalene-1-yl) -4-quinazolinone, fomitoside-K, mevastatin and AZD8055 (an mTOR inhibitor), and their biological mechanisms of apoptosis (48)(49)(50)(51)(52)(53)(54)(55). Consistent with the present results, an antitumor role of JNK has been proposed upon treatment of HNSCC cells with the JNK inhibitor SP600125, which diminished the aforementioned pharmacological agents-induced apoptosis (47)(48)(49)(50)(51)(52)(53)(54). Similarly, Li and Johnson (56) demonstrated that pharmacological inhibition of JNK with SP600125 markedly inhibited bortezomib-induction of autophagy regulatory proteins and autophagosome formation in HNSCC.…”

Section: Discussionmentioning

confidence: 99%

JNK1/2 expression and modulation of STAT3 signaling in oral cancer

et al. 2016

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Abstract. Mitogen-activated protein kinases (MAPKs) are a family of protein kinases that link extracellular stimuli with intracellular responses and participate in numerous cellular processes such as growth, proliferation, differentiation, inflammation and apoptosis. Persistent activation of signal transducer and activator of transcription 3 (STAT3), which is accompanied by increases in STAT3 tyrosine phosphorylation, is associated with cell proliferation, differentiation and apoptosis in oral squamous cell carcinoma (OSCC). The role and significance of the activation of MAPKs, particularly of c-Jun N-terminal kinase (JNK), on STAT3 signaling in OSCC have not been thoroughly investigated. The present study examines the effects of JNK1/2 modulation on STAT3 signaling and cellular activities in OSCC cells. The expression levels of STAT3 [total, tyrosine phosphorylated (p-Tyr) and serine phosphorylated (p-Ser)], JNK, c-Jun and cyclin D1 were assessed in the OSCC cell lines SCC25 and SCC9. Inhibition of JNK1/2 was achieved by pharmacological agents (SP600125) and by small interfering RNA (siRNA) silencing, while JNK1/2 was induced by active MAPK kinase 7. Cell proliferation and viability rates were also evaluated. Inhibition of JNK1/2 with either SP600125 treatment or specific siRNA silencing resulted in decreased levels of p-Ser STAT3 and increased levels of p-Tyr STAT3 and cyclin D1 in both cell lines. Furthermore, JNK1/2 inhibition resulted in a dose-dependent increase in cell growth and viability in both cell lines. Opposite results were observed with JNK1/2 induction in both cell lines. The present results are supportive of a potential tumor suppressive role of JNK1/2 signaling in OSCC, which may be mediated through negative crosstalk with the oncogenic STAT3 signaling pathway. The possible therapeutic implications of JNK1/2 inhibition for patients with OSCC require to be investigated.

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5-aminolevulinic acid induce apoptosis via NF-κB/JNK pathway in human oral cancer Ca9-22 cells

Abstract: These results demonstrate significant involvement of caspase-8 and -9 and their upstream NF-κB-JNK pathways in ALA-PDT-induced apoptosis. Future studies on how NF-κB and JNK activity regulate ALA-PDT response should provide a better strategy for the treatment of oral cancer.

Cited by 37 publications

References 32 publications

Synergistic Anticancer Activity of 5-Aminolevulinic Acid Photodynamic Therapy in Combination with Low-dose Cisplatin on Hela Cells

Synergistic Anticancer Activity of 5-Aminolevulinic Acid Photodynamic Therapy in Combination with Low-dose Cisplatin on Hela Cells

Dihydroartemisinin Increases the Sensitivity of Photodynamic Therapy Via NF-κB/HIF-1α/VEGF Pathway in Esophageal Cancer Cell in vitro and in vivo

JNK1/2 expression and modulation of STAT3 signaling in oral cancer

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