Jia-He Wang

ShenJing Hospital of China Medical University, Feng-t’ien, Liaoning, China

Are you Jia-He Wang?

Claim your profile

Publications (16)18.76 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Breast cancer is one of the most common cancers in women in the world. Health-related quality of life (HRQL) at treatment endpoint in cancer clinical trials is widely considered to be increasingly important. The aim of this review was to provide a literature-based assessment of the validity, reliability and responsiveness of breast cancer-specific HRQL instruments in women breast cancer patients. Materials and Methods: The databases consulted were Medline, PubMed, and Embase. The inclusion criteria required studies to: (1) involve use of HRQL measures; (2) cover women with breast cancer under standard treatment (surgery, radiation therapy, chemotherapy, hormone therapy, and targeted therapy); (3) involve the validity, reliability, or responsiveness of HRQL; (4) deal with validation of breast cancer-specific HRQL instruments. Results: A total of 16 studies were identified through the literature search that met the 4 inclusion criteria. Some seven instruments were assessed among these 16 studies: EORTC QLQ-BR23, FACT-B, FACT-ES, HFRDIS, LSQ- 32, QLICP-BR, and SLDS-BC. EORTC QLQ-BR23, FACT-B, LSQ-32, QLICP-BR, and SLDS-BC are more general breast cancer-specific HRQL instruments. FACT-EB is the endocrine subscale combined with FACT-B in order to measure the side effects and putative benefits of hormonal treatment administered in breast cancer patients. HFRDIS is the HRQL measure focusing on hot flash concerns. Conclusions: This paper provides an overall understanding on the currently available breast cancer-specific HRQL instruments in women breast cancer patients.
    Asian Pacific journal of cancer prevention: APJCP 01/2014; 15(8):3533-6. · 1.27 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pseudolaric acid B (PAB) is a diterpene acid isolated from the root and trunk bark of Pseudolarix kaempferi Gordon (Pinaceae). Recent studies have reported that PAB exhibits cytotoxic effects in several cancer cell lines. In the present study, we assessed its antitumor activity and molecular mechanisms in HO-8910 and A2780 ovarian cancer cells in vitro. We found that PAB reduced cell viability and induced apoptosis in a dose- and time-dependent manner in HO-8910 and A2780 human ovarian cancer cells. The induction of apoptosis was also accompanied by the regulation of Bcl-2 and XIAP family proteins, cytochrome c and Apaf-1. Moreover, we observed that PAB treatment resulted in the activation of caspase-3 and -9, which may partly explain the anticancer activity of PAB. Collectively, the present study for the first time suggests that PAB enhances apoptosis of HO-8910 and A2780 cells through regulation of Bcl-2 and IAP family proteins. Moreover, the triggering of caspase-3 and -9 activation mediated apoptotic induction. Our results suggest that PAB may be a new therapeutic option for the treatment of ovarian cancers.
    Oncology Reports 11/2013; · 2.30 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Numerous studies have demonstrated that pseudolaric acid B (PAB) promotes apoptosis in several cancer cell lines. However, thus far, the effect of PAB on human leukemia cells has not been evaluated. In the present study, the antitumor activity and molecular mechanisms of PAB in human leukemia U937 cells were investigated. It was demonstrated that PAB induced U937 cell apoptosis, which was confirmed by typical morphological changes and Annexin V‑fluorescein isothiocyanate staining. PAB was observed to activate a caspase‑dependent apoptotic pathway in U937 cells through the regulation of the Bcl‑2 family protein-mediated mitochondrial pathway. Furthermore, the activities of caspase‑3 and -9 were increased following treatment with PAB. In conclusion, to the best of our knowledge, this study demonstrated for the first time that PAB was able to enhance the apoptosis of U937 cells, at least in part, through the activation of the mitochondrial death pathway. Moreover, the activation of caspase‑3 and -9 mediated the apoptotic induction.
    Molecular Medicine Reports 07/2013; · 1.17 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The invasion of Staphylococcus aureus into alveolar epithelial cells is regarded as the key step for S. aureus lung infection. However, the mechanism of internalization of S. aureus by alveolar epithelial cells is not clear, and was the aim of this investigation Human lung adenocarcinomic epithelial cells and A549 cells were used. Human β1 integrin and rat β1 integrin were detected by real-time reverse transcription (RT)-PCR. The expressions of β1 integrin, Akt and p-Akt were detected by Western blot analysis. To further investigate the role of β1 integrin in S. aureus internalization by alveolar epithelial cells, we next performed siRNA-mediated knockdown of β1 integrin expression. In this study, we found that S. aureus invades human alveolar epithelial cells and rat primary alveolar epithelial cells. The β1 integrin ligand competitive inhibitor, GRGDS-peptide, blocked the internalization of S. aureus by A549 cells. Knockdown of β1 integrin also inhibited the internalization of S. aureus. In addition, the PI3K/Akt signaling pathway in alveolar epithelial cells was activated by the infection with S. aureus. Furthermore, Akt phosphorylation was abolished by transient transfection with β1 integrin siRNA in A549 cells challenged with S. aureus. Our results suggest that the phosphatidylinositol 3-kinase/Akt signaling pathway plays an important role in β1 integrin-mediated internalization of S. aureus by alveolar epithelial cells.
    The Journal of Microbiology 06/2013; · 1.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The herb of Hedyotis diffusa Willd (H. diffusa Willd), an annual herb distributed in northeastern Asia, has been known as a traditional oriental medicine for the treatment of cancer. Recently, Chinese researchers have discovered that two anthraquinones isolated from a water extract of H. diffusa Willd showed apoptosis-inducing effects against cancer cells. However, the cellular and molecular mechanisms responsible for this phenomenon are poorly understood. The current study determines the role of mitogen-activated protein kinases (MAPK) in human leukemic U937 cells apoptosis induced by 2-hydroxy-3-methylanthraquinone from H. diffusa. Our results showed that 2-hydroxy-3-methylanthraquinone decreased phosphorylation-ERK1/2 (p-ERK1/2), and increased p-p38MAPK, but did not affect expressions of p-JNK1/2 in U937 cells. Moreover, treatment of U937 cells with 2-hydroxy-3-methylanthraquinone resulted in activation of caspase-3. Furthermore, PD98059 (ERK1/2 inhibitor) significantly enhanced 2-hydroxy-3-methylanthraquinone-induced apoptosis in U937 cells, whereas caspase-3 inhibitor or SB203580 (p-p38MAPK inhibitor), decreased apoptosis in U937 cells. Taken together, our study for the first time suggests that 2-hydroxy-3-methylanthraquinone is able to enhance apoptosis of U937 cells, at least in part, through activation of p-p38MAPK and downregulation of p-ERK1/2. Moreover, the triggering of caspase-3 activation mediated apoptotic induction.
    Archives of Pharmacal Research 04/2013; · 1.54 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Jolkinolide B from the roots of Euphorbia fischeriana Steud exhibits significant antitumor activities against several tumor lines. Previous study has shown that Jolkinolide B could induce apoptosis in human leukemia cells. However, the exact mechanism and signaling pathway involved in Jolkinolide B-induced apoptosis have not been fully elucidated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in dose- and time-dependent manner in human leukemic HL-60 and THP-1 cells. The induction of apoptosis was accompanied by the downregulation of JAK2/STAT3. Our results also suggest that expression of Bcl-2 and mitochondrial cytochrome c was dosedependently reduced following Jolkinolide B-treated THP-1 and HL-60 cells, whereas Jolkinolide B up-regulated the expression of Bax and cytosolic cytochrome c. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3, -8, and -9. JSI-124, a STAT-3 inhibitor, was able to block the negative effect of Jolkinolide B on cell apoptosis. Taken together, our study for the first time suggests that Jolkinolide B is able to enhance apoptosis of human leukemic HL-60 and THP-1 cells, at least in part, through downregulation of JAK2/STAT3 and bcl-2, and upregulation of Bax and cytosolic cytochrome c. Moreover, the triggering of caspase-3, -8, and -9 activation mediated apoptotic induction.
    International journal of clinical pharmacology and therapeutics 12/2012; · 1.20 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ganoderma lucidum (Lingzhi) is traditionally drug, which has been traditionally effective used in the treatment of chronic hepatopathy, hypertension, hyperglycemia and cancer. THP-1 and HL-60 apoptosis induced by active lipids of Ganoderma lucidum spores was quantified by flow cytometry using FITC-conjugated annexin V and PI; MAPK and Akt were measured by Western blot, and caspase-3, -8 and -9 activities were also detected by spectrophotometric assay. Our results showed that active lipids of Ganoderma lucidum spores decreased phosphorylation-ERK1/2 (P-ERK1/2), P-Akt and increased P-JNK1/2, but did not affect expressions of P-p38 MAPK in THP-1 cells. Moreover, treatment of THP-1 cells with active lipids of Ganoderma lucidum spores resulted in activation of caspase-3, -8 and -9. Furthermore, LY294002 (Akt inhibitor) or PD98059 (ERK1/2 inhibitor) significantly enhanced active lipids of Ganoderma lucidum spores-induced apoptosis in THP-1 cells, whereas caspase inhibitors or SP600125 (JNK inhibitor), decreased apoptosis in THP-1 cells. Taken together, our study for the first time suggests that active lipids of Ganoderma lucidum spores is able to enhance apoptosis in THP-1 cells, at least in part, through inhibition of ERK1/2, Akt and activation of JNK1/2 signaling pathways. Moreover, it also triggers caspase-3, -8 and -9 activation mediated apoptotic induction.
    Journal of ethnopharmacology 12/2011; 139(2):582-9. · 2.32 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Numerous studies have shown that Hedyotis diffusa WILLD (H. diffusa) could promote apoptosis in several cancer cell lines. However, the cellular and molecular mechanisms responsible for this phenomenon are still poorly understood. The current study determines the role of Fas/FasL in THP-1 cell apoptosis induced by 2-hydroxy-3-methylanthraquinone from H. diffusa. THP-1 cells were treated with 2-hydroxy-3-methylanthraquinone from H. diffusa. The effect on the cell viability of THP-1 cells was evaluated using the trypan blue assay, and cell apoptosis was measured by Giemsa staining and flow cytometry. Protein expression was assayed using the Western blot method. Our results showed that 2-hydroxy-3-methylanthraquinone from H. diffusa induced THP-1 cell apoptosis in a time- and dose-dependent manner. Apoptosis was associated with a more prominent induction expression of Fas/FasL, DR4 and TRAIL in a time-dependent manner. Moreover, treatment of THP-1 cells with 2-hydroxy-3-methylanthraquinone from H. diffusa resulted in activation of caspase-8. For the first time, our study suggests that 2-hydroxy-3-methylanthraquinone from H. diffusa is able to enhance apoptosis of THP-1 cells, at least in part, through activation of Fas/FasL, DR4 and TRAIL. Moreover, triggering of caspase-8 activation mediated apoptotic induction.
    Archives of medical research 11/2011; 42(7):577-83. · 1.88 Impact Factor
  • Jia-He Wang, Yi-Jun Zhou, Xue Bai, Ping He
    [Show abstract] [Hide abstract]
    ABSTRACT: Jolkinolide B, a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud, is known to induce apoptosis in cancer cells. However, the molecular mechanism of its anti-cancer activity has not been fully elucidated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in a dose- and time-dependent manner in human leukemic U937. The induction of apoptosis was also accompanied by the downregulation of PI3K/Akt and the inhibitor of apoptosis protein (IAP) family proteins. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3 and -9, which may partly explain the anti-cancer activity of Jolkinolide B. Taken together, our study for the first time suggest that Jolkinolide B is able to enhance apoptosis of U937 cells, at least in part, through downregulation of PI3K/Akt and IAP family proteins. Moreover, triggering of caspase-3 and -9 activation mediated apoptotic induction.
    Molecules and Cells 11/2011; 32(5):451-7. · 2.21 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Apoptosis is a genetically regulated cellular suicide mechanism that plays an essential role in development and in defense of multicellular organism. Escherichia coli (E. coli) can induce monocyte apoptosis; however, the mechanism is not clear. This study determines if Fas/FasL regulates E. coli-induced human monocyte line U937 cell apoptosis. We found that infection of U937 cells with E. coli induced rapid cell death in a dose- and time-dependent manner displaying the characteristic features of apoptosis. Moreover, opsonized E. coli induced U937 apoptosis with a higher apoptotic rate (53.29 ± 5.83%) than non-opsonized E. coli (19.37 ± 2.56%). Studying the underlying mechanisms we found that the E. coli-induced apoptosis was associated with a more prominent induction expression of Fas/FasL in a time- and dose-dependent manner. Furthermore, E. coli treatment resulted in a significant increase in the levels of DR5, TRAIL, and FADD, but exerted no statistically significant effects on the levels of DR4. The activity of caspase-8 enzyme increased in infection groups, positively correlated with apoptosis rate. Taken together, these results clearly indicate that receptor-mediated phagocytosis of E. coli induces apoptosis. Moreover, our findings suggest a possible regulatory role of Fas/FasL in the pathway of E. coli infection.
    Molecular and Cellular Biochemistry 06/2011; 358(1-2):95-104. · 2.33 Impact Factor
  • Jia-He Wang, Bo Yu, Ping He, Xue Bai
    [Show abstract] [Hide abstract]
    ABSTRACT: We previously showed that infection of human monocytic U937 cells with nonpathogenic Escherichia coli (E. coli) induced rapid apoptosis in a dose- and time-dependent manner. We also found that E. coli increase p38 mitogen-activated protein Kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK), and decrease extracellular-Regulated Kinase1/2 (ERK1/2) phosphorylation and increase caspase-3 and -9 activity in U937 cells. The current study determines if Bcl-2, Bax, the phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factor kappa B (NF-κB) regulates E. coli–induced U937 cell apoptosis. Studying the underlying mechanisms we found that the E. coli-induced apoptosis in U937 cells was associated with a more prominent reduction in expression of Bcl-2, levels of P-Akt and NF-κB. Because levels of inhibition of apoptosis protein (cIAP), and X-chromosomelinked inhibitor of apoptosis protein (XIAP) are regulated by NF-κB, E. coli decreased the levels of these proteins in U937 cells through inhibition of NF-κB. Moreover, E. coli markedly elevated Bax expression and cytochrome c redistribution. LY294002, PDTC and Embelin, specific inhibitors of PI3K, NF-κB and XIAP, induced U937 cell apoptosis and the apoptosis is dependent on activity of caspase-3 and -9 in E. coli-treated U937 cells. Through using LY294002 and western blotting, we identified NF-κB was the downstream Akt target regulated by E. coli. Taken together, these results clearly indicate reduced activation of NF-κB via impaired PI3K/Akt activation could result in increased apoptosis of U937 cells infected by E. coli. Moreover, E. coli can induce apoptosis with an increased expression of Bax and a reduced expression of Bcl-2, which resulted in increased levels of cytochrome c release and increase caspase-3 and -9 in U937 cells. Keywords E. coli –Apoptosis–U937–Bcl-2–NF-κB–PI3K/Akt–Caspase
    World Journal of Microbiology and Biotechnology 01/2011; 27(8):1827-1838. · 1.26 Impact Factor
  • Jia-he Wang, Yi-jun Zhou, Li Tian, Ping He
    [Show abstract] [Hide abstract]
    ABSTRACT: To explore the mechanisms involved in Staphylococcus aureus (S. aureus) invading human monocytic U937 cells. S. aureus were added to U937 cells at multiplicity of infections (MOI) of 20:1 for 0, 15, 30, 60, and 90 minutes, respectively. Cell apoptosis was analyzed with Hoechst 33258 staining and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry analysis. Akt and nuclear factor-kappaB (NF-kappaB) activities were detected by Western blotting. Infection of U937 cells with S. aureus induced rapid cell death in a time-dependent manner, and the cells displayed characteristic features of apoptosis. S. aureus-induced apoptosis was associated with a prominent downregulation of activated (phosphorylated) Akt and NF-kappaB. The inhibition of phosphorylated Akt by LY294002 led to the inhibition of NF-kappaB in a dose-dependent manner. Inhibition of Akt with LY294002 caused further increase in apoptosis of U937 cells. S. aureus can stimulate the apoptosis of U937 cells. S. aureus induces apoptosis of U937 cells by inhibiting Akt-regulated NF-kappaB.
    Chinese Medical Sciences Journal 12/2009; 24(4):231-5.
  • [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the effect of SP600125, a specific c-jun N-terminal protein kinase (JNK) inhibitor, on Staphylococcus aureus (S. aureus)-induced U937 cell death and the underlying mechanism. The human monocytic U937 cells were treated with S. aureus at different time with or without SP600125. Cell apoptosis was analyzed by flow cytometry. JNK, Bax, and caspase-3 activities were detected by Western blotting. S. aureus induced apoptosis in cultured U937 cells in a time-dependent manner. Expression of Bax and phospho-JNK significantly increased in S. aureus-treated U937 cells, and the level of activated caspase-3 also increased in a time-dependent manner. Inhibition of JNK with SP600125 significantly inhibited S. aureus-induced apoptosis in U937 cells. S. aureus can induce apoptosis in U937 cells by phosphorylation of JNK and activation of Bax and caspase-3. SP600125 protects U937 cells from apoptosis induced by S. aureus via inhibiting the activity of JNK.
    Chinese Medical Sciences Journal 04/2009; 24(1):26-9.
  • Jia-he Wang, Yi-jun Zhou, Li Tian, Ping He
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective To explore the mechanisms involved in Staphylococcus aureus (S. aureus) invading human monocytic U937 cells. Methods S. aureus were added to U937 cells at multiplicity of infections (MOI) of 20:1 for 0, 15, 30, 60, and 90 minutes, respectively. Cell apoptosis was analyzed with Hoechst 33258 staining and Annexin V- fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry analysis. Akt and nuclear factor-κB (NF-κB) activities were detected by Western blotting. Results Infection of U937 cells with S. aureus induced rapid cell death in a time-dependent manner, and the cells displayed characteristic features of apoptosis. S. aureus-induced apoptosis was associated with a prominent downregulation of activated (phosphorylated) Akt and NF-κB. The inhibition of phosphorylated Akt by LY294002 led to the inhibition of NF-κB in a dose-dependent manner. Inhibition of Akt with LY294002 caused further increase in apoptosis of U937 cells. Conclusions S. aureus can stimulate the apoptosis of U937 cells. S. aureus induces apoptosis of U937 cells by inhibiting Akt-regulated NF-κB.
    Chinese Medical Sciences Journal 01/2009; 24(4):231-235.
  • [Show abstract] [Hide abstract]
    ABSTRACT: To investigate whether the effect of E. coli on U937 cell lines apoptosis is mediated via p38 mitogen-activated protein kinase (MAPK) activation. The U937 cell lines were treated with E. coli at different time or together with SB203580, an inhibitor for p38. Cell apoptosis was analyzed by flow cytometry. p38 activities were detected by Western blotting. E. coli induced apoptosis in cultured U937 cell lines in a time-dependent manner. The phosphorylation of p38 was induced after 10 minutes infection, reached the peak after 20 minutes, and started to decline after 30 minutes. In contrast, the level of total p38 protein was not changed in whole experimental period. Inhibition of p38 with SB203580 significantly inhibited E. coli induced apoptosis in U937 cells. The activation of the p38 MAPK in U937 cell lines by E. coli is a major pathway to mediate the apoptosis.
    Chinese Medical Sciences Journal 04/2007; 22(1):49-53.
  • Yi-jun Zhou, Jia-he Wang, Jin Zhang
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the effects of hepatocyte growth factor (HGF) on vascular endothelial cells apoptosis induced by advanced glycation end products (AGEs) and its possible mechanism. Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and intervened by different concentrations of AGEs and HGF. The cell inhibitory rates of each group with different culture time (12, 24, 48, and 72 hours) were measured by methyl thiazolyl tetrazolium (MTT) assay. The early stage apoptosis was detected by flow cytometry with Annexin V-FITC/PI double staining, morphology of cell apoptosis was observed by hoechst 33258 fluorescence staining, and the expression of apoptosis-associated genes Bax and Bcl-2 were determined by Western blotting. The activity of caspase-3 was detected by enzyme-linked immunosorbent assay (ELISA). Morphological observation indicated that high concentration of AGEs induced characteristic apoptotic changes in HUVECs. Within a certain concentration range, HUVECs apoptosis inducing rates by AGEs were in both dose- and time-dependent manners. HGF significantly inhibited the apoptosis of HUVECs induced by AGEs (P < 0.05). AGEs significantly promoted expression of Bax protein, but not Bcl-2. Whereas HGF significantly promoted the expression of Bcl-2 (P < 0.01) and decreased the activity of caspase-3 (P < 0.05) without affecting Bax level. AGEs can induce the apoptosis of endothelial cells in vitro. HGF may effectively attenuate AGEs-induced endothelial cells apoptosis through upregulating Bcl-2 gene expression and inhibiting caspase-3 activation.
    Chinese Medical Sciences Journal 04/2006; 21(1):6-10.