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RISS 인기검색어
- 검색키워드
- 저자 : Min Xianglan (검색결과 7 건)
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The Effect of Disintegrin–Metalloproteinase ADAM9 in Gastric Cancer Progression
Kim, Jeong Min,Jeung, Hei-Cheul,Rha, Sun Young,Yu, Eun Jeong,Kim, Tae Soo,Shin, You Keun,Zhang, Xianglan,Park, Kyu Hyun,Park, Seung Woo,Chung, Hyun Cheol,Powis, Garth American Association for Cancer Research 2014 Molecular Cancer Therapeutics Vol.13 No.12
<P>Advanced gastric cancer is one of the most aggressive gastrointestinal malignancies, and ADAM (A disintegrin and metalloproteinase)-9 is a cell-surface membrane glycoprotein with oncogenic properties that is overexpressed in several cancers. Herein, we investigated the biologic mechanism of ADAM9 in the progression, proliferation, and invasion of gastric cancer. First, we detected ADAM's expression, processing, and protease activity in gastric cancer cells. Protease activity was moderately correlated with ADAM9 protein expression, but was better related to a processed smaller molecular weight (84 kDa) form of ADAM9. Knockdown of ADAM9 or specifically targeted monoclonal antibody (RAV-18) suppressed cancer cell proliferation and invasion in high ADAM9-expressing cells, not in low ADAM9-expressing cells. RAV-18 showed <I>in vivo</I> antitumor activity in a gastric cancer xenograft model. Hypoxia (1% oxygen) induced ADAM9 expression and functional activity in low ADAM9-expressing gastric cancer cells that was inhibited by siRNA knockdown or RAV-18 antibody to levels in normoxic cells. Overall, our studies show that ADAM9 plays an important role in gastric cancer proliferation and invasion, and that while expressed in some gastric cancer cells at high levels that are responsive to functional inhibition and antitumor activity of a catalytic site–directed antibody, other gastric cancer cells have low levels of expression and only when exposed to hypoxia do ADAM9 levels increase and the cells become responsive to ADAM9 antibody inhibition. Therefore, our findings suggest that ADAM9 could be an effective therapeutic target for advanced gastric cancer. <I>Mol Cancer Ther; 13(12); 3074–85. ©2014 AACR</I>.</P>
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Analysis of evolutionary and genetic patterns in structural genes of primate lentiviruses
Cho Myeongji,Min Xianglan,Son Hyeon S. 한국유전학회 2022 Genes & Genomics Vol.44 No.7
Background: Primate lentiviruses (HIV1, HIV2, and Simian immunodeficiency virus [SIV]) cause immune deficiency, encephalitis, and infectious anemia in mammals such as cattle, cat, goat, sheep, horse, and puma. Objective: This study was designed and conducted with the main purpose of confirming the overall codon usage pattern of primate lentiviruses and exploring the evolutionary and genetic characteristics commonly or specifically expressed in HIV1, HIV2, and SIV. Methods: The gag, pol, and env gene sequences of HIV1, HIV2, and SIV were analyzed to determine their evolutionary relationships, nucleotide compositions, codon usage patterns, neutrality, selection pressure (influence of mutational pressure and natural selection), and viral adaptation to human codon usage. Results: A strong 'A' bias was confirmed in all three structural genes, consistent with previous findings regarding HIV. Notably, the ENC-GC3s plot and neutral evolution analysis showed that all primate lentiviruses were more affected by selection pressure than by mutation caused by the GC composition of the gene, consistent with prior reports regarding HIV1. The overall codon usage bias of pol was highest among the structural genes, while the codon usage bias of env was lowest. The virus groups showing high codon bias in all three genes were HIV1 and SIVcolobus. The codon adaptation index (CAI) and similarity D(A, B) values indicated that although there was a high degree of similarity to human codon usage in all three structural genes of HIV, this similarity was not caused by translation pressure. In addition, compared with HIV1, the codon usage of HIV2 is more similar to the human codon usage, but the overall codon usage bias is lower. Conclusion: The origin viruses of HIV (SIVcpz_gor and SIVsmm) exhibit greater similarity to human codon usage in the gag gene, confirming their robust adaptability to human codon usage. Therefore, HIV1 and HIV2 may have evolved to avoid human codon usage by selection pressure in the gag gene after interspecies transmission from SIV hosts to humans. By overcoming safety and stability issues, information from codon usage analysis will be useful for attenuated HIV1 vaccine development. A recoded HIV1 variant can be used as a vaccine vector or in immunotherapy to induce specific innate immune responses. Further research regarding HIV1 dinucleotide usage and codon pair usage will facilitate new approaches to the treatment of AIDS.
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Bae, Jung Yoon,Kim, Eun Kyoung,Yang, Dong Hyun,Zhang, Xianglan,Park, Young-Jin,Lee, Doo Young,Che, Chung Min,Kim, Jin Neoplasia Press 2014 Neoplasia Vol.16 No.11
<P>Crosstalk between cancer cells and carcinoma-associated fibroblasts (CAFs) has earned recognition as an interaction that plays a pivotal role in carcinogenesis. Thus, we attempted to clarify whether increase in the level of CAFs promotes cancer progression by proportionally enhancing the interaction between cancer cells and CAFs. We first analyzed clinical correlation between the levels of fibroblasts and cancer progression and found that the level of CAFs made a noticeable difference on the prognosis of patients with oral squamous cell carcinoma (OSCC). <I>In vivo</I> animal study also demonstrated that tumor volume depended on the dose of CAFs that was co-injected with OSCC cells. The same tendency was observed in an <I>in vitro</I> study. We also found that interleukin-1α (IL-1α) secreted from OSCC cells had dual effects on CAFs: IL-1α not only promoted the proliferation of CAFs but also upregulated the secretion of cytokines in CAFs such as CCL7, CXCL1, and IL-8. The induction activity of cytokine secretion by IL-1α surpassed that of proliferation in OSCC cells. In summary, we unraveled an important interactive mechanism of carcinogenesis: IL-1α released from carcinoma stimulates the proliferation of CAFs and the simultaneous increase in cytokine secretion from CAFs promotes cancer progression in human OSCC. On the basis of these findings, we propose that the level of CAFs is eligible for being selected as a prognostic factor that will be useful in routine diagnosis. We also propose that blockage of reciprocal interaction between cancer cells and CAFs will provide an insight for developing novel chemotherapeutic strategy.</P>
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Jun, Ikhyun,Park, Hyung Soon,Piao, He,Han, Jung Woo,An, Min Ji,Yun, Byeong Gyu,Zhang, Xianglan,Cha, Yong Hoon,Shin, You Keun,Yook, Jong In,Jung, Jinsei,Gee, Heon Yung,Park, Joon Seong,Yoon, Dong Sup,J Nature Publishing Group 2017 The British journal of cancer Vol. No.
<P><B>Background:</B></P><P>Anoctamin (ANO)/transmembrane member 16 (TMEM16) proteins mediate diverse physiological and pathophysiological functions including cancer cell proliferation. The present study aimed to identify the role of ANOs in pancreatic cancer.</P><P><B>Methods:</B></P><P>In an initial screen of ANOs, ANO9/TMEM16J was overexpressed in pancreatic cancer cells, and its role in the pathogenesis of pancreatic cancer was evaluated using an integrated <I>in vitro</I> and <I>in vivo</I> approach. To determine clinical relevance of the experimental findings, the prognostic value of ANO9 was evaluated in patients with pancreatic cancer.</P><P><B>Results:</B></P><P>The ANO9 mRNA and protein levels were increased in pancreatic cancer-derived cells. Exogenous expression of <I>ANO9</I> in PANC-1 cells significantly increased cell proliferation in cell cultures and in mice. In contrast, knockdown of <I>ANO9</I> in AsPC-1, BxPC-3, and Capan-2 cells strongly inhibited cell proliferation. Mechanistic analysis suggested that physical association of ANO9 with epidermal growth factor receptor (EGFR) underlies ANO9-induced cell proliferation. Knockdown <I>of ANO9</I> augmented the effects of the EGFR inhibitor and the cytotoxic agent on pancreatic cancer cell proliferation. In addition, high ANO9 expression is a poor prognostic factor in patients with pancreatic cancer.</P><P><B>Conclusions:</B></P><P>The ANO9/TMEM16J appears to be a clinically useful prognostic marker for pancreatic cancer and a potential therapeutic target.</P>
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