siRNA targeting midkine inhibits gastric cancer cells growth and induces apoptosis involved caspase-3,8,9 activation and mitochondrial depolarization

Wang, Qingling; Huang, Yue; Ni, Yanhong; Wang, Hui; Hou, Yayi

doi:10.1007/s11373-007-9192-0

Cited by 28 publications

(20 citation statements)

References 24 publications

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“…This protein is overexpressed in various human malignancies, including bladder, prostate, breast, lung, liver, and colon tumors, although its expression is typically low or undetectable in normal adult tissues (8 -10). In tumors, MDK exhibits angiogenic (11), mitogenic (12), and antiapoptotic activities (13). Its expression in tumors (8,14) and its concentration in plasma (15) are associated with a poor disease outcome.…”

Section: Midkine (Mdk)mentioning

confidence: 99%

The Signal Peptide of the Tumor-shared Antigen Midkine Hosts CD4+ T Cell Epitopes

Kerzerho¹,

Schneider²,

Favry³

et al. 2013

Journal of Biological Chemistry

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Background: The CD4 T cell response to the tumor antigen Midkine was unknown. Results: Most of the T cell response to Midkine relies on T cell epitopes contained in its signal peptide. Conclusion:The signal peptide of Midkine is accessible to HLA class II pathway for CD4 T cell presentation. Significance: It is a new function for signal peptides to contribute to tumor-specific CD4 T cell response.

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Section: Midkine (Mdk)mentioning

confidence: 99%

The Signal Peptide of the Tumor-shared Antigen Midkine Hosts CD4+ T Cell Epitopes

Kerzerho¹,

Schneider²,

Favry³

et al. 2013

Journal of Biological Chemistry

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“…We previously also found that MK was highly expressed in the gastric tumor tissues of Chinese patients and patients with malignant effusions [25, 26]. Both siRNA targeting MK gene and the conjugate (a single-chain variable fragment against human MK-Doxorubicin) inhibited gastric cancer cell growth and induced apoptosis [27, 28]. MK is therefore an attractive molecular target for cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

Dihydroartemisinin and Curcumin Synergistically Induce Apoptosis in SKOV3 Cells Via Upregulation of MiR-124 Targeting Midkine

Zhao

Pan

et al. 2017

Cell Physiol Biochem

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Background/Aim: Women with advanced ovarian carcinoma are less likely to receive platinum-based chemotherapy and surgery due to a greater risk of cytotoxicity and poorer outcomes. We attempted to improve a promising therapy against ovarian cancer by using a combination of dihydroartemisinin (DHA) and curcumin (Cur). Methods: Human ovarian cancer SKOV3 cells were treated with DHA, Cur alone, or a combination of both. The viability of SKOV3 cells was measured by Cell Counting Kit-8 (CCK-8) and a colony formation assay. The cell cycle and apoptosis of SKOV3 cells were monitored by flow cytometry. The mRNA and protein expression levels of target genes were respectively examined by qRT-PCR and western blot. The biological effects of miR-124 on midkine (MK) were verified by a luciferase activity analysis. Results: Combined treatment of DHA and Cur synergistically decreased cell viability, arrested cell cycle, and promoted apoptosis in SKOV3 cells. Moreover, it significantly attenuated the expression of oncogene MK and synergistically upregulated the expression of miR-124. Furthermore, miR-124 was verified to bind directly to the 3ʹ-untranslated region of MK mRNA, resulting in mRNA degradation and reduced MK protein levels. The combination of DHA with Cur significantly inhibited tumor growth in xenograft nude mice without obvious toxicity. Conclusion: Co-treatment with DHA and Cur exhibited a synergistic anti-tumor effect on SKOV3 cells both in vitro and in vivo.

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“…Based on the fact that in normal developing mouse embryos MK gene and protein play a role in cell differentiation and organogenesis [25] , these results suggested that MK mRNA and protein along with ER-β mRNA and protein may have some relationship to the lung cancer cell differentiation in NSCLC. Another earlier study [28] in our lab indicated that small interfering RNA (siRNA) targeting MK gene can inhibit gastric cancer cell growth and induce apoptosis via mitochondrial depolarization and caspase-3 activation, which suggested that MK siRNA may be a promising novel and potential therapeutic strategy for the treatment of gastric cancers. Therefore, MK siRNA should also be a good candidate for treating NSCLC.…”

Section: Discussionmentioning

confidence: 95%

Increased midkine and estrogen receptor-β expression in human non-small cell lung cancer

Zhang

Zhao

Huang

et al. 2009

Chin. J. Cancer Res.

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Objective: Midkine (MK), a new member of the heparin-binding growth factor family, has been found recently to have a high expression level in many tumor specimens including lung carcinoma. Estrogens may be involved in lung carcinogenesis, and estrogen receptors, mainly estrogen receptor-β (ER-β), are present and functional in normal lung and tumor cell lines and tissues. In addition, estrogens and growth factors may promote the progression of human non-small cell lung cancer (NSCLC). Previously, we have immunohistochemically demonstrated that MK and ER-β proteins were overexpressed in NSCLC and their expression levels were both significantly negatively correlated with the pathological classification. The purpose of this study was to further verify their expression and its correlation with NSCLC.Methods: Taking NSCLC tissues and their corresponding paraneoplastic and normal lung as research objects, we further examined the expression of MK and ER-β by meas of RT-PCR, in situ hybridization and Western blot analyses at the levels of messenger RNA (mRNA) and protein, respectively.Results: The increased MK and ER-β mRNA expression was found in NSCLC by RT-PCR and in situ hybridization analyses. Furthermore, Western blot analysis also displayed increased expression of MK and ER-β proteins in NSCLC. Finally, their correlation analysis at the levels of mRNA and protein expression in NSCLC demonstrated that MK protein level was significantly correlated to estrogen receptor-β (P<0.01, r s =0.535); in spite of their correlation at the mRNA level, there was no remarkable difference between MK and ER-β (P>0.05, r s =0.178).Conclusion: All these results in the present study confirmed that MK and ER-β were overexpressed in human NSCLC.

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siRNA targeting midkine inhibits gastric cancer cells growth and induces apoptosis involved caspase-3,8,9 activation and mitochondrial depolarization

Cited by 28 publications

References 24 publications

The Signal Peptide of the Tumor-shared Antigen Midkine Hosts CD4+ T Cell Epitopes

The Signal Peptide of the Tumor-shared Antigen Midkine Hosts CD4+ T Cell Epitopes

Dihydroartemisinin and Curcumin Synergistically Induce Apoptosis in SKOV3 Cells Via Upregulation of MiR-124 Targeting Midkine

Increased midkine and estrogen receptor-β expression in human non-small cell lung cancer

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