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RISS 인기검색어
- 검색키워드
- 저자 : Perumal Elumalai (검색결과 4 건)
- 무료
- 기관 내 무료
- 유료
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Review on Molecular and Chemopreventive Potential of Nimbolide in Cancer
Perumal Elumalai,Jagadeesan Arunakaran 한국유전체학회 2014 Genomics & informatics Vol.12 No.4
Cancer is the most dreaded disease in human and also major health problem worldwide. Despite its high occurrence, theexact molecular mechanisms of the development and progression are not fully understood. The existing cancer therapybased on allopathic medicine is expensive, exhibits side effects; and may also alter the normal functioning of genes. Thus, anon-toxic and effective mode of treatment is needed to control cancer development and progression. Some medicinal plantsoffer a safe, effective and affordable remedy to control the cancer progression. Nimbolide, a limnoid derived from the neem(Azadirachta indica) leaves and flowers of neem, is widely used in traditional medical practices for treating various humandiseases. Nimbolide exhibits several pharmacological effects among which its anticancer activity is the most promising. Theprevious studies carried out over the decades have shown that nimbolide inhibits cell proliferation and metastasis of cancercells. This review highlights the current knowledge on the molecular targets that contribute to the observed anticanceractivity of nimbolide related to induction of apoptosis and cell cycle arrest; and inhibition of signaling pathways related tocancer progression.
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Review on Molecular and Chemopreventive Potential of Nimbolide in Cancer
Elumalai, Perumal,Arunakaran, Jagadeesan Korea Genome Organization 2014 Genomics & informatics Vol.12 No.4
Cancer is the most dreaded disease in human and also major health problem worldwide. Despite its high occurrence, the exact molecular mechanisms of the development and progression are not fully understood. The existing cancer therapy based on allopathic medicine is expensive, exhibits side effects; and may also alter the normal functioning of genes. Thus, a non-toxic and effective mode of treatment is needed to control cancer development and progression. Some medicinal plants offer a safe, effective and affordable remedy to control the cancer progression. Nimbolide, a limnoid derived from the neem (Azadirachta indica) leaves and flowers of neem, is widely used in traditional medical practices for treating various human diseases. Nimbolide exhibits several pharmacological effects among which its anticancer activity is the most promising. The previous studies carried out over the decades have shown that nimbolide inhibits cell proliferation and metastasis of cancer cells. This review highlights the current knowledge on the molecular targets that contribute to the observed anticancer activity of nimbolide related to induction of apoptosis and cell cycle arrest; and inhibition of signaling pathways related to cancer progression.
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Perumal, Elumalai,So Youn, Kim,Sun, Shin,Seung-Hyun, Jung,Suji, Min,Jieying, Liu,Yeun-Jun, Chung Elsevier 2019 Lung cancer Vol.130 No.-
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>Epithelial-mesenchymal transition (EMT) is the key event in distant metastasis of diverse tumors including lung cancer. Recent evidence suggests the involvement of phosphatase and tensin homolog (PTEN) in EMT phenotypes. However, the molecular mechanism of EMT induced by PTEN inactivation is not clear in lung cancer. We aimed to investigate the role of PTEN inactivation in acquisition of EMT in lung cancer cells.</P> <P><B>Methods</B></P> <P>We knocked out the PTEN in PTEN proficient lung cancer cells lines (A549 and NCI-H460) using CRISPR/Cas-9 system and observed the growth, EMT phenotypes, and EMT related molecules. We also explored the in vivo effect of PTEN inactivation on tumor cell growth and distant metastasis using nude mouse injection.</P> <P><B>Results</B></P> <P>PTEN knockout (KO) cells showed faster growth, migration and invasion than PTEN wild-type (WT) cells. When we injected the cells into nude mice, PTEN-KO cells showed faster growth and higher metastatic potential. In PTEN-KO cells, the levels of phosphorylated AKT (Ser-473 and Thr-308) were profoundly elevated and the expressions of phosphorylated GSK-3β (Ser9, inactive form) increased, while that of β-catenin decreased. Regarding the EMT markers, the expression of E-cadherin decreased but those of N-cadherin, vimentin and MMP-2 increased in the PTEN-KO cells. Especially, PTEN-KO cells showed the almost complete intra-nuclear shift of β-catenin and no β-catenin signal was observed in the cell membrane. Accordingly, PTEN-KO cells exhibited morphological changes such as loss of cell-to-cell contact, pseudopodia and the round shape, which are the typical phenotypes of EMT. Snail and Slug were also dominantly accumulated in the nucleus after PTEN inactivation.</P> <P><B>Conclusion</B></P> <P>All these data consistently support that PTEN inactivation contributes to EMT by nuclear translocation of β-catenin and Snail/Slug in lung cancer cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Epithelial-mesenchymal transition (EMT) is behind tumor invasion and metastasis. </LI> <LI> We examined the role of PTEN inactivation in EMT in lung cancer cells. </LI> <LI> Inactivated PTEN affects EMT by nuclear translocation of β-catenin and Snail/Slug. </LI> <LI> PI3K/AKT/GSK-3β pathway was essential for inducing EMT in PTEN inactivated cells. </LI> </UL> </P>
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