Mitogen-Activated Protein Kinase Signal Transduction in Solid Tumors

Lei, Yuanyuan; Wang, Weijia; Mei, Jinhong; Wang, Chunliang

doi:10.7314/apjcp.2014.15.20.8539

Cited by 81 publications

(67 citation statements)

References 111 publications

(137 reference statements)

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“…c-Jun N-terminal kinase (JNK) is a member of the MAPK family, and is associated with the regulation of cell proliferation, survival and differentiation [25]. Recent studies have demonstrated that JNK is involved in mediating the apoptotic response of cells to pro-inflammatory cytokines and environmental stresses in most cases [26,27]. Meanwhile, ROS has been demonstrated to be involved in the regulation of apoptosis [28] and the sustained phosphorylation of JNK (p-JNK) [24].…”

Section: Introductionmentioning

confidence: 99%

Raddeanin a Suppresses Glioblastoma Growth by Inducing ROS Generation and Subsequent JNK Activation to Promote Cell Apoptosis

Peng

Wang

Shu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Raddeanin A (RA), an active pharmacological ingredient from Anemone raddeana Regel, plays an important role in tumor suppression. In this study, we assessed the potentially therapeutic effect of RA on glioblastoma and its underlying mechanisms. Methods: Cell viability was examined using the MTT assay. Invasive and migratory capacities were examined using Transwell and wound healing assays. Apoptosis was determined by Hoechst staining, flow cytometry, DCFH-fluorescent probe and immunohistochemical staining. Autophagy was detected by transmission electron microscopy and western blotting. A U251 glioma xenograft model was established to evaluate the effect of RA in vivo. Results: The data demonstrated that RA inhibited viability, and abrogated the invasive/migratory abilities of glioblastoma cells. In addition, RA induced apoptosis by reactive oxygen species (ROS)/ Jun N-terminal kinase (JNK) signaling in glioblastoma. Conversely, the antioxidant N-Acetyl-L-cysteine (NAC) and pan-caspase inhibitor z-VAD-fmk attenuated RA-induced apoptosis by scavenging ROS and inactivating caspase-3. Furthermore, the inhibition of autophagy by 3-MA exacerbated apoptosis through ROS generation and JNK phosphorylation. In vivo, RA exhibited a curative effect on U251-derived xenografts in nude mice. Conclusions: The results of this study suggest that RA suppressed the growth of glioblastoma, thus serving as a promising and potential strategy for glioblastoma chemotherapy.

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Section: Introductionmentioning

confidence: 99%

Raddeanin a Suppresses Glioblastoma Growth by Inducing ROS Generation and Subsequent JNK Activation to Promote Cell Apoptosis

Peng

Wang

Shu

et al. 2018

Cell Physiol Biochem

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“…Triptolide has been suggested to have anti-cancer, anti-inflammatory, immunosuppressive and anti-cystogenic activity (5). MKP-1 protein is often overexpressed in tumors and is considered to be related to chemoresistance (12,13). Cancer cells express high levels of Hsps that are closely correlated with poor prognosis (25).…”

Section: Discussionmentioning

confidence: 99%

“…MKP-1 is an endogenous MAPK deactivator. MKP-1 is often overexpressed in tumors and is considered to be related to the failure of various chemotherapeutics (12,13).…”

Section: Introductionmentioning

confidence: 99%

Triptolide reduces the viability of osteosarcoma cells by reducing MKP-1 and Hsp70 expression

Zhao

Jiang

Wang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Osteosarcoma is the most common type of malignant bone tumor found in adolescents and young adults. The aim of the present study was to determine whether triptolide, a diterpene epoxide extracted from the Tripterygium plant, was able effectively decrease the viability of osteosarcoma cells. The underlying molecular mechanisms are also investigated. The human osteosarcoma cell lines U-2 OS and MG-63 were used in this study. The U-2 OS and MG-63 cells were treated with 0, 5, 10, 25 or 50 nM triptolide. Cells treated with dimethyl sulfoxide only were used as the no drug treatment control. A commercial MTT kit was used to determine the effects of triptolide on cells. Mitogen-activated protein kinase phosphatase-1 (MKP-1) is frequently overexpressed in tumor tissues, possibly related to the failure of a number of chemotherapeutics. Heat shock protein 70 (Hsp70) is a chaperone molecule that is able to increase drug resistance. The protein expression levels of MKP-1 and Hsp70 were determined using western blot analysis. The results indicate that triptolide effectively reduced the viability of the osteosarcoma cells. Furthermore, triptolide was found to effectively reduce MKP-1 expression and Hsp70 levels. Further analysis showed that triptolide reduced MKP-1 mRNA expression in the U-2 OS and MG-63 cells. Triptolide reduced Hsp70 mRNA expression levels in U-2 OS and MG-63 cells. These results suggest that triptolide effectively decreases the viability of osteosarcoma cells. These effects may be associated with the decreased expression of MKP-1 and Hsp70 levels. These results suggest that triptolide may be used in the treatments of osteosarcoma.

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“…The mitogen activated protein kinases (MAPK) signal pathway is one of the main signaling pathways involved in immune responses, with vital roles in the regulation of cytokine and chemokine responses (32). There are three main components in the MAPK signaling pathway: The Jun N-terminal kinase (JNK 1/2/3), extracellular signal-regulated kinase (ERK1/2, ERK 3/4, ERK5, ERK 7/8,) and p38 MAPKs (p38α/β/γ/δ) (33)(34)(35)(36). Once stimulated, the MAPKs, which are expressed in all cell types, are activated and participate in various physiological and biologic processes including inflammation, growth, differentiation, survival and apoptosis of cells (35)(36)(37).…”

Section: Expression and Regulation Of Il-37mentioning

confidence: 99%

“…There are three main components in the MAPK signaling pathway: The Jun N-terminal kinase (JNK 1/2/3), extracellular signal-regulated kinase (ERK1/2, ERK 3/4, ERK5, ERK 7/8,) and p38 MAPKs (p38α/β/γ/δ) (33)(34)(35)(36). Once stimulated, the MAPKs, which are expressed in all cell types, are activated and participate in various physiological and biologic processes including inflammation, growth, differentiation, survival and apoptosis of cells (35)(36)(37). Phosphatidylinositol 3-kinases (PI3Ks) are a family of lipid kinases that play important roles in intracellular signal transduction and regulation of inflammatory and immune processes (38,39).…”

Section: Expression and Regulation Of Il-37mentioning

confidence: 99%

Interleukin-37: A crucial cytokine with multiple roles in disease and potentially clinical therapy (Review)

et al. 2018

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Abstract. Interleukin (IL)-37, a new IL-1 family member, has received increasing attention in recent years. In the past decade, it has been determined that IL-37 is expressed in various normal cells and tissues and is regulated by inflammatory stimuli and pro-cytokines via different signal transduction pathways. Recently, it has been found that IL-37 is expressed in a variety of cancers, chronic inflammatory and autoimmune disorders, and exerts anti-inflammatory effects. Moreover, a growing body of literature demonstrates that IL-37 plays a vital role in inhibiting both innate and adaptive immune responses as well as inflammatory reactions. In addition, IL-37 may prove to be a new and potentially useful target for effective cytokine therapy. Further evidence is needed to clarify in more detail the effects of IL-37 in experimental and clinical studies. Based on an extensive summary of published data, the aim of this review is to outline the current knowledge of IL-37, including the location, structure, expression, regulation and function, as well as the potential clinical applications of this cytokine.

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Mitogen-Activated Protein Kinase Signal Transduction in Solid Tumors

Cited by 81 publications

References 111 publications

Raddeanin a Suppresses Glioblastoma Growth by Inducing ROS Generation and Subsequent JNK Activation to Promote Cell Apoptosis

Raddeanin a Suppresses Glioblastoma Growth by Inducing ROS Generation and Subsequent JNK Activation to Promote Cell Apoptosis

Triptolide reduces the viability of osteosarcoma cells by reducing MKP-1 and Hsp70 expression

Interleukin-37: A crucial cytokine with multiple roles in disease and potentially clinical therapy (Review)

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