Apoptotic effect of 3,4‐dihydroxybenzoic acid on human gastric carcinoma cells involving JNK/p38 MAPK signaling activation

Lin, Hui-Hsuan; Chen, Jing-Hsien; Huang, Chi‐Chou; Wang, Chau‐Jong

doi:10.1002/ijc.22571

Cited by 128 publications

(81 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The Martin-Perez group demonstrated that this was due in part to activation of mitogen-activated protein kinases (MAPK) by lauryl gallate (2c) and, more particularly, the ERK1/2 kinases (Table 1) [29]. Protocatechuic acid (3) was capable of stimulating c-Jun N-terminal kinase (JNK), another p38 MAPK, and as a consequence induced cell death in HepG2 hepatocellular carcinoma and AGS human gastric adenocarcinoma cells (Table 1) [30,31]. Caffeic and ferulic derivatives (5, 6 and 7) target specifically the PKC protein kinase family and arrest growth of various cancer cells, such as for example U937 human leukemic cells (Table 1) [18,32,33].…”

Section: Group I: Polyphenolic Acids and Their Analoguesmentioning

confidence: 99%

Natural Polyphenols that Display Anticancer Properties through Inhibition of Kinase Activity

Lamoral-Theys¹,

Pottier

Dufrasne³

et al. 2010

CMC

124

View full text Add to dashboard Cite

Over eleven hundred publications reporting anticancer activities of polyphenols have appeared in the peerreviewed literature. In addition, a search of the PubMed database using "polyphenols -cancer -review" as keywords produced over 320 hits for review articles (July 2009). Polyphenol anticancer activities include, among others, anti-oxidative, pro-apoptotic, DNA damaging, anti-angiogenic, and immunostimulatory effects. Targeting specific protein kinases to combat cancer represents a major focus of oncology research within the so-called targeted therapy approach. An exhaustive search of the PubMed database (July 2009) using "polyphenols -cancer -kinases" as keywords resulted in more than 130 hits, half of them having been published within the past five years. Furthermore, the PubMed database contains 25 reviews on the subject of anti-kinase activity of some specific polyphenols, including mainly curcumin and the green tea polyphenol (-)-epigallocatechin 3-gallate (EGCG). However, no attempt has been made yet to review this area of research in a comprehensive, general manner. The current review therefore aims to highlight those anticancer polyphenols that target specific kinases in various types of cancer. The present review also provides an in-depth analysis of polyphenol structure-activity relationships in relation to their anticancer activities and specific kinase targeting. Lastly, a number of polyphenols are identified as potential antitumor agents that could be used to combat biologically aggressive cancers, including metastasizing cancers, through the targeting of specific kinases.

show abstract

Section: Group I: Polyphenolic Acids and Their Analoguesmentioning

confidence: 99%

Natural Polyphenols that Display Anticancer Properties through Inhibition of Kinase Activity

Lamoral-Theys¹,

Pottier

Dufrasne³

et al. 2010

CMC

124

View full text Add to dashboard Cite

show abstract

“…It is a main metabolite of complex polyphenols, especially anthocyanins, which are converted to PCA and also abundantly formed and absorbed in the large intestine because of microbial metabolization (Kay et al 2005, Vitaglione et al 2007. Previous reports of both in vitro and in vivo studies have demonstrated that PCA has anti-carcinogen (Tseng et al 2000, Yip et al 2006, Lin et al 2007), antihyperglycemia , Harini & Pugalendi 2010, antioxidant (Liu et al 2002, Sroka & Cisowski 2003, Masella et al 2004, Shi et al 2006, Tarozzi et al 2007, Chou et al 2010, Zhang et al 2011, and anti-inflammatory properties (Yan et al 2004, Min et al 2010, Wang et al 2010. However, no scientific investigation has yet been conducted on the effect of PCA on diabetes-induced cardiac dysfunction, which is also caused by oxidative stress, and thus this investigation was conducted to study the anti-hyperglycemic activity of PCA and the effect of PCA on diabetes-induced cardiac dysfunction and other related metabolic parameters in STZ-induced diabetic rats.…”

Section: Introductionmentioning

confidence: 99%

Protocatechuic acid exerts a cardioprotective effect in type 1 diabetic rats

Semaming¹,

Kumfu²,

Pannangpetch³

et al. 2014

Journal of Endocrinology

View full text Add to dashboard Cite

Oxidative stress has been shown to play an important role in the pathogenesis of diabetesinduced cardiac dysfunction. Protocatechuic acid (PCA) is a phenolic compound, a main metabolite of anthocyanin, which has been reported to display various pharmacological properties. We proposed the hypothesis that PCA exerts cardioprotection in type 1 diabetic (T1DM) rats. T1DM was induced in male Sprague-Dawley rats by a single i.p. injection of 50 mg/kg streptozotocin (STZ) and groups of these animals received the following treatments for 12 weeks: i) oral administration of vehicle, ii) oral administration of PCA at a dose of 50 mg/kg per day, iii) oral administration of PCA at a dose of 100 mg/kg per day, iv) s.c. injection of insulin at a dose of 4 U/kg per day, and v) a combination of PCA, 100 mg/kg per day and insulin, 4 U/kg per day. Metabolic parameters, results from echocardiography, and heart rate variability were monitored every 4 weeks, and the HbA1c, cardiac malondialdehyde (MDA), cardiac mitochondrial function, and cardiac BAX/BCL2 expression were evaluated at the end of treatment. PCA, insulin, and combined drug treatments significantly improved metabolic parameters and cardiac function as shown by increased percentage fractional shortening and percentage left ventricular ejection fraction and decreased low-frequency:high-frequency ratio in T1DM rats. Moreover, all treatments significantly decreased plasma HbA1c and cardiac MDA levels, improved cardiac mitochondrial function, and increased BCL2 expression. Our results demonstrated for the first time, to our knowledge, the efficacy of PCA in improving cardiac function and cardiac autonomic balance, preventing cardiac mitochondrial dysfunction, and increasing anti-apoptotic protein in STZ-induced T1DM rats. Thus, PCA possesses a potential cardioprotective effect and could restore cardiac function when combined with insulin treatment. These findings indicated that supplementation with PCA might be helpful for the prevention and alleviation of cardiovascular complications in T1DM.

show abstract

“…JNK activation is also regulated by scaffold proteins, JNKinteracting protein (JIP) and JNK stress-activated protein kinaseassociated protein 1 (JSAP1) (Whitmarsh et al, 1998;Ito et al, 1999). Depending on the cell type and the stimulus, JNK can activate a number of diverse downstream targets including members of the activator protein-1 (AP-1) family, c-Jun, JunD, activating transcriptional factor 2 (ATF2), Bcl-2 proteins, c-Myc and p53 (Bode and Dong, 2007;Lin et al, 2007). Whether JNK induces or suppresses apoptosis is largely dependent on the molecules it activates.…”

mentioning

confidence: 99%

Differential activation of JNK1 isoforms by TRAIL receptors modulate apoptosis of colon cancer cell lines

et al. 2009

View full text Add to dashboard Cite

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis on binding to its receptors, death receptor 4 and 5 (DR4, DR5). TRAIL can also activate c-Jun N-terminal kinase (JNK) through the adaptor molecules, TNF receptor-associated factor 2 (TRAF2) and receptor-interacting protein (RIP). The role of JNK in TRAIL-induced tumour cell apoptosis is unclear. In this study, we demonstrate that JNK is activated by TRAIL in colon cancer cells. Inhibition of JNK with L-JNKI reduced rhTRAIL-induced cell death but enhanced cell death induced by selective activation of DR4 or DR5. This difference was unrelated to receptor internalisation or differential activation of c-Jun, but activation of different JNK isoforms. Our data demonstrate that JNK1, but not JNK2 is activated by rhTRAIL in the examined colon cancer cell lines. Although rhTRAIL activated both the long and short isoforms of JNK1, selective activation of DR4 or DR5 led to predominant activation of the short JNK1 isoforms (JNK1a1 and/or JNK1b1). Knockdown of JNK1a1 by shRNA enhanced apoptosis induced by TRAIL, agonistic DR4 or DR5 antibodies. On the other hand, knockdown of the long JNK1 isoforms (JNK1a2 and JNK1b2) had the opposite effect; it reduced TRAIL-induced cell death. These data indicate that the short JNK1 isoforms transmit an antiapoptotic signal, whereas the long isoforms (JNK1a2 or JNK1b2) act in a proapoptotic manner.

show abstract

Apoptotic effect of 3,4‐dihydroxybenzoic acid on human gastric carcinoma cells involving JNK/p38 MAPK signaling activation

Cited by 128 publications

References 46 publications

Natural Polyphenols that Display Anticancer Properties through Inhibition of Kinase Activity

Natural Polyphenols that Display Anticancer Properties through Inhibition of Kinase Activity

Protocatechuic acid exerts a cardioprotective effect in type 1 diabetic rats

Differential activation of JNK1 isoforms by TRAIL receptors modulate apoptosis of colon cancer cell lines

Contact Info

Product

Resources

About