Ganoderma atrum polysaccharide evokes antitumor activity via cAMP-PKA mediated apoptotic pathway and down-regulation of Ca(2+)/PKC signal pathway.
Ganoderma atrum polysaccharide (PSG-1) has been commonly suggested as a candidate for prevention and therapy of cancer. We investigated the antitumor effect and the underlying molecular mechanisms of PSG-1. The results showed that PSG-1 inhibited tumor growth and resulted in tumor cell apoptosis in vivo. Here, the data revealed that PSG-1 caused a markedly increase in cAMP and PKA activities, rather than cGMP and PKC. Moreover, the treatment of PSG-1 induced a dramatic increase in the protein level of PKA. In contrast, the expression of PKC and intracellular [Ca(2+)]i were inhibited. Our study also revealed that treatment with PSG-1 increased the spleen and thymus weights, lymphocyte proliferation and macrophage phagocytic activity in tumor-bearing mice. Taken together, we conclude that PSG-1 could inhibit the tumor growth, possibly in part by enhancing the induction of apoptosis through cAMP-PKA signaling pathway and down-regulation of Ca(2+)/PKC signal pathway, activating host immune function in S180-bearing mice.
State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi 330047, China.
Shenshen
S
Zhang
State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi 330047, China. Electronic address: spnie@ncu.edu.cn.
Shaoping
S
Nie
State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi 330047, China.
Danfei
D
Huang
State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi 330047, China.
Jianqin
J
Huang
State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi 330047, China.
Yanling
Y
Feng
State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang, Jiangxi 330047, China. Electronic address: myxie@ncu.edu.cn.
Mingyong
M
Xie
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D000242:Cyclic AMP / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000235:genetics / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects; D005260:Female; D032902:Ganoderma / Q000737:chemistry*; D008264:Macrophages / Q000187:drug effects; D051379:Mice; D009369:Neoplasms / Q000188:drug therapy; D011134:Polysaccharides / Q000494:pharmacology*; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D013154:Spleen / Q000166:cytology / Q000187:drug effects
D000970:Antineoplastic Agents; D011134:Polysaccharides; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D006152:Cyclic GMP
Antitumor; Apoptosis; Ganoderma atrum polysaccharide; Protein kinase A; Protein kinase C