Nm23-H1 was involved in regulation of KAI1 expression in high-metastatic lung cancer cells L9981

You, Jiacong; Chang, R. P. H.; Liu, Bin; Zu, Lingling; Zhou, Qinghua

doi:10.21037/jtd.2016.04.59

Cited by 12 publications

(10 citation statements)

References 35 publications

(31 reference statements)

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“…70 Further, KAI-1 expression was regulated through Nm23-H1 through modulation of KAI-1 promoter activity in L9981 lung cancer cells. 71 Another study showed that c-Myc can upregulate the expression of Nm23-H1. 72 Furthermore, the oncoprotein ErbB2 expression was shown to be regulated by Nm23-H1, which affects the cell proliferative activity of ErbB2.…”

Section: Transcription Regulation Of Cellular Targets By Nm23 H1mentioning

confidence: 99%

Oncogenic Epstein–Barr virus recruits Nm23-H1 to regulate chromatin modifiers

Pandey

Robertson

2018

Laboratory Investigation

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In cancer progression, metastasis is a major cause of poor survival of patients and can be targeted for therapeutic interventions. The first discovered metastatic-suppressor Nm23-H1 possesses nucleoside diphosphate kinase, histidine kinase, and DNase activity as a broad-spectrum enzyme. Recent advances in cancer metastasis have opened new ways for the development of therapeutic molecular approaches. In this review, we provide a summary of the current understanding of Nm23/NDPKs in the context of viral oncogenesis. We also focused on Nm23-H1-mediated cellular events with an emphasis on chromatin modifications. How Nm23-H1 modulates the activities of chromatin modifiers through interaction with Epstein–Barr virus-encoded oncogenic antigens and related crosstalks are discussed in the context of other oncogenic viruses. We also described the current understanding of the cellular and viral interactions of Nm23-H1 and their reference to transcription regulation and metastasis. Further, we summarized the recent therapeutic approaches targeting Nm23 and its potential links to pathways that can be exploited by oncogenic viruses.

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Section: Transcription Regulation Of Cellular Targets By Nm23 H1mentioning

confidence: 99%

Oncogenic Epstein–Barr virus recruits Nm23-H1 to regulate chromatin modifiers

Pandey

Robertson

2018

Laboratory Investigation

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“…The gene encoding NM23-H1 is a suppressor of tumor metastasis; research has revealed that it may reduce MMP-2 and -9 expression in various types of cancer cells (18)(19)(20)(21)35,42,43). Boissan et al (19) previously reported that NM23-H1 silencing promotesthe extracellular matrix invasion of HepG2 cells by up regulating numerous MMPs, including MMP-2.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…When transfected with NM23 genes, a variety of tumor cell types were reported to exhibit the inhibition of metastatic properties, including migration, invasion, and colonization (14-18). The NM23-H1 (NME1) gene was reported to be the one closely associated with the metastasis of cancer cells, including breast, lung and liver cancer (19)(20)(21).Lindera aggregata (Sims) Kosterm is a traditional Chinese herbal medicine often used in Asia. It has been used to treat chest and abdominal pain, indigestion, regurgitation, colds, hernia and frequent urination (22 Abbreviations: MMP-2, matrix metalloproteinase-2; ILL, isolinderalactone; FOXO3, transcriptional factor fork head box O3; STAT3, signal transducer and activator of transcription 3; CUM, curcumin; DMSO, dimethyl sulfoxide; Nm23-H1, NME/NM23 nucleoside diphosphate kinase 1…”

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confidence: 99%

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Anti-metastatic effects of isolinderalactone via the inhibition of MMP-2 and up regulation of NM23-H1 expression in human lung cancer A549 cells

et al. 2018

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Abstract. Metastatic lung cancer is a leading cause of mortality and has a mortality rate of ≥90%. Isolinderalactone (ILL) is a sesquiterpene lactone compound that has been used in traditional Chinese medicine. Research has demonstrated that ILL has anti-inflammatory and anti-proliferative properties; however, to the best of our knowledge, studies investigating whether ILL can inhibit lung cancer cell metastasis have not been conducted. In the present study, 1-10 µM ILL was applied in the culturing of the A549 lung cancer cell line to investigate the effects of ILL on the invasion and migration of lung cancer cells, including whether the possible mechanisms of ILL are associated with the expression of matrix metalloproteinase (MMP)-2 and NME/NM23 nucleoside diphosphate kinase 1 (NM23-H1) genes. The results of the present study indicated that ILL inhibited the invasion and migration of the A549 cancer cells and exhibited a dose-response association. ILL also significantly inhibited the protein expression and activity of MMP-2 (P<0.05), exhibiting a trend similar to that of its invasion-and migration-associated properties. Further research revealed that ILL significantly increased the expression of NM23-H1 protein and inhibited the expression of β-catenin protein (P<0.05). The results of the present study is, to the best of our knowledge, the first to confirm that ILL can inhibit the invasion and migration of A549 cancer cells, with the possible mechanisms potentially involving the inhibition of MMP-2 and β-catenin protein expression resulting from the up regulation of NM23-H1 expression. IntroductionCancer is a leading cause of mortality; ~8.2 million people worldwide succumbed to cancer-associated mortality in 2012, with lung cancer accounting for ~1.59 million cases of mortality, or ~20% of the total (1). Lung cancer cell metastasis is a primary cause of mortality and those that experience it have a mortality rate of ≥90% (2). When it metastasizes, lung cancer has a 95% chance of affecting local lymph nodes and an 80% chance of affecting other organs (3,4). Thus, in clinical terms, the overall 5-year survival rate from the time of diagnosis to mortality for patients with lung cancer undergoing treatment is only 10-15% (5). Cancer cell metastasis is a complex multistep process involving invasion and migration (6-8). Matrix metalloproteinases (MMPs) are zinc/calcium-dependent endopeptidases involved in the degradation of the extracellular matrix, two examples of which are MMP-2 and -9 (7,9). MMP-2 is a notable factor in the development of tumor metastasis (7,10). MMP-2 is highly expressed in malignant tumors and serves a key role in cancer invasion and angiogenesis (7,11). The inhibition of MMP-2 is, therefore, an effective strategy for preventing tumor cell metastasis (11,12). The NME/NM23 nucleoside diphosphate kinase 1 (NM23) gene was first identified in the murine melanoma cell line exhibiting high metastatic activity; increasing the expression of this gene may also reduce the metastatic activity of tumor cel...

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“…The function of nm23 in human cancer is currently unconfirmed (22,(28)(29)(30)(31), and certain reports have indicated there is a link between high expression of the nm-23 gene and its protein product with low metastatic potential of cancer (28). Nm-23 is known to be associated with early onset of familial breast and ovarian cancer (28).…”

Section: Discussionmentioning

confidence: 99%

Inhibition effects of Yuxiao San combined with cisplatin on transplanted tumor growths via upregulation of nm‑23 and downregulation of K‑ras in Lewis lung cancer mice

et al. 2018

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Traditional Chinese medicine applied to cancer therapy has a long history. This study aimed to investigate the effect and underlying mechanism of the traditional Chinese medicine, Yuxiao San, in combination with cisplatin, on Lewis lung cancer mice. Lewis lung cancer mouse models were were established in mice, and were randomly divided into model (normal saline + egg white), cisplatin (cisplatin injection + egg white), traditional Chinese medicine (Yuxiao San + egg white) and combined medication (Yuxiao San + cisplatin injection + egg white) groups. The weight and tumor size of mice was measured every 3 days, and the number of lung surface metastasis nodules were calculated after 14 days. Nucleoside diphosphate kinase (nm-23) and K-ras expression levels in tumor tissues were determined by immunohistochemical methods and reverse transcriptionquantitative polymerase chain reaction. The results suggested that compared with the model group, cisplatin, traditional Chinese medicine and combined medication groups significantly inhibited growth of transplanted tumors, reduced the number of lung metastasis nodules, increased the inhibition rate of lung metastasis (P<0.05 or P<0.01), significantly increased tumor suppressor gene nm-23 expression and significantly downregulated oncogene K-ras expression. Among all groups, the effect of the combined medication group for inhibiting tumor growth was most favorable (P<0.01). Compared with the cisplatin group, nm-23 expression in the traditional Chinese medicine group and the combined medication group was significantly increased, and K-ras expression in the traditional Chinese medicine and combined medication groups was significantly reduced (P<0.01). To conclude, Yuxiao San and cisplatin injection effectively inhibited growth of the transplanted tumor. The underlying mechanism may be associate with nm-23 upregulation and K-ras downregulation. Therefore, the Yuxiao San and cisplatin injection may become a potential therapeutic strategy for tumor treatment.

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Nm23-H1 was involved in regulation of KAI1 expression in high-metastatic lung cancer cells L9981

Cited by 12 publications

References 35 publications

Oncogenic Epstein–Barr virus recruits Nm23-H1 to regulate chromatin modifiers

Oncogenic Epstein–Barr virus recruits Nm23-H1 to regulate chromatin modifiers

Anti-metastatic effects of isolinderalactone via the inhibition of MMP-2 and up regulation of NM23-H1 expression in human lung cancer A549 cells

Inhibition effects of Yuxiao San combined with cisplatin on transplanted tumor growths via upregulation of nm‑23 and downregulation of K‑ras in Lewis lung cancer mice

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