Anti-proliferative effect of honokiol in oral squamous cancer through the regulation of specificity protein 1

Kim, Dong-Wook; Ko, Seon Mi; Jeon, Young‐Joo; Noh, Young-Woock; Choi, Nak Hwan; Cho, Sung‐Dae; Moon, Hong Seop; Cho, Young Sik; Shin, Jae-Chen; Park, Seon‐Min; Seo, Kang Seok; Choi, Ji-Young; Chae, Jung‐Il; Shim, Jung‐Hyun

doi:10.3892/ijo.2013.2028

Cited by 35 publications

(27 citation statements)

References 45 publications

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“…According to our previous report, Sp1 is an essential transcription factor for OSCC tumorigenesis (23). Therefore, we reasoned that Sp1 protein might be a target for regulating growth of OSCC.…”

Section: Lca Suppresses Sp1 Expression In Osccmentioning

confidence: 93%

“…The levels of both Sp1 protein and caspase-3 were gradually decreased with times by LCA. The Sp1 protein governs the downstream targets including p27, p21, cyclin D1, Mcl-1 and survivin, dysregulated expression of which causes apoptosis and cell cycle arrest in various cancer cells (20,23). Cell cycle arrest proteins such as p27 and p21 were elevated in HN22 (Fig.…”

Section: Lca Suppresses Sp1 Expression In Osccmentioning

confidence: 99%

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Licochalcone A, a natural chalconoid isolated from Glycyrrhiza inflata root, induces apoptosis via Sp1 and Sp1 regulatory proteins in oral squamous cell carcinoma

Cho

Chae

Yoon

et al. 2014

International Journal of Oncology

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Abstract. Licochalcone A (LCA), a chalconoid derived from root of Glycyrrhiza inflata, has been known to possess a wide range of biological functions such as antitumor, antiangiogenesis, antiparasitic, anti-oxidant, antibacterial and anti-inflammatory effects. However, the anticancer effects of LCA on oral squamous cell carcinoma (OSCC) have not been reported. Our data showed that LCA inhibited OSCC cell (HN22 and HSC4) growth in a concentration-and timedependent manner. Mechanistically, it was mediated via downregulation of specificity protein 1 (Sp1) expression and subsequent regulation of Sp1 downstream proteins such as p27, p21, cyclin D1, Mcl-1 and survivin. Here, we found that LCA caused apoptotic cell death in HSC4 and HN22 cells, as characterized by sub-G 1 population, nuclear condensation, Annexin V staining, and multi-caspase activity and apoptotic regulatory proteins such as Bax, Bid, Bcl-xl , caspase-3 and PARP. Consequently, this study strongly suggests that LCA induces apoptotic cell death of OSCC cells via downregulation of Sp1 expression, prompting its potential use for the treatment of human OSCC.

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Section: Lca Suppresses Sp1 Expression In Osccmentioning

confidence: 93%

Section: Lca Suppresses Sp1 Expression In Osccmentioning

confidence: 99%

Licochalcone A, a natural chalconoid isolated from Glycyrrhiza inflata root, induces apoptosis via Sp1 and Sp1 regulatory proteins in oral squamous cell carcinoma

Cho

Chae

Yoon

et al. 2014

International Journal of Oncology

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“…As honokiol exhibits anticancer effects in different cancer types (6,(24)(25)(26)(27)(28), its effect on the growth of human RCC was evaluated in this study. A-498 and 786-0 cells were treated with honokiol (0-80 µM) for 24 h and proliferation was determined as described in ʻMaterials and methodsʼ.…”

Section: Effect Of Honokiol On the Proliferation And Viability Of Rccmentioning

confidence: 99%

Honokiol inhibits migration of renal cell carcinoma through activation of RhoA/ROCK/MLC signaling pathway

Cheng

Castillo

Welty

et al. 2016

International Journal of Oncology

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Abstract. Honokiol, a biologically active compound isolated from Magnolia bark, has been shown to possess promising anticancer effect through induction of apoptosis. However, there is a relative lack of information regarding its anti-metastatic activity. Renal cell carcinoma (RCC) is the most common malignancy of the adult kidney and is known for high risk of metastasis. Clinically, therapeutic methods for metastatic RCC cases are limited and efforts to exploit new treatments are still ongoing. The results of our current investigation first revealed that honokiol suppressed the proliferation of different human RCCs without affecting cell viability. In addition, honokiol inhibited migration of highly metastatic RCC 786-0 cells and stimulated the activity of small GTPase, RhoA. Furthermore, phosphorylated myosin light chain (MLC) and excessive formation of actin stress fibers were identified in 786-0 cells treated with honokiol. Interestingly, the pharmacological Rho-associated protein kinase (ROCK) inhibitor Y-27632 attenuated contraction of actin stress fibers induced by honokiol and abrogated honokiol-mediated inhibition of cell migration. Together these important findings suggest that honokiol suppresses the migration of highly metastatic RCC through activation of RhoA/ROCK/MLC signaling and warrants attention in the treatment of RCC metastasis as a novel therapeutic approach.

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“…28,29) In particular, Sp1 is known to mediate prostaglandin E2-and nicotine-induced growth of NSCLC cells, 30,31) and we show that Sp1 is significantly reduced in cells treated with β-lap and that cell cycle-and apoptosis-related proteins are regulated by Sp1.…”

Section: Discussionmentioning

confidence: 88%

Beta-Lapachone Suppresses Non-small Cell Lung Cancer Proliferation through the Regulation of Specificity Protein 1

Jeon

Bang

Choi

et al. 2015

Biological & Pharmaceutical Bulletin

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Lung cancer is the leading cause of cancer-related death worldwide, and non-small cell lung cancer (NSCLC) is the most common pathological type with a reported frequency of about 85% of all cases. Despite recent advances in therapeutic agents and targeted therapies, the prognosis for NSCLC remains poor, and therefore it is important to identify the biological targets of this complex disease since a blockade of such targets would affect multiple downstream signaling cascades. β-Lapachone (β-Lap) is an antiproliferative agent that selectively induces apoptosis-related cell death in a variety of human cancer cells. However, the mechanisms of its action require further investigation. In this study, we show that treatment with β-lap triggers apoptosis and cell-cycle arrest in two NSCLC cell lines: H1299 and NCI-H358. The transcription factor specificity protein 1 (Sp1) was markedly inhibited by β-lap in a dose-and time-dependent manner. Furthermore, β-lap modulated the protein expression levels of the Sp1 regulatory genes, including cell-cycle regulatory proteins and antiapoptotic proteins, resulting in apoptosis. Taken together, our results indicate that β-lap may be a potential antiproliferative agent candidate by inducing apoptotic cell death in NSCLC tissue through downregulation of Sp1.

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Anti-proliferative effect of honokiol in oral squamous cancer through the regulation of specificity protein 1

Cited by 35 publications

References 45 publications

Licochalcone A, a natural chalconoid isolated from Glycyrrhiza inflata root, induces apoptosis via Sp1 and Sp1 regulatory proteins in oral squamous cell carcinoma

Licochalcone A, a natural chalconoid isolated from Glycyrrhiza inflata root, induces apoptosis via Sp1 and Sp1 regulatory proteins in oral squamous cell carcinoma

Honokiol inhibits migration of renal cell carcinoma through activation of RhoA/ROCK/MLC signaling pathway

Beta-Lapachone Suppresses Non-small Cell Lung Cancer Proliferation through the Regulation of Specificity Protein 1

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