Aberrant Expression Levels of MTA1 and RECK in Nasopharyngeal Carcinoma: Association with Metastasis, Recurrence, and Prognosis

Deng, Yan; Zhou, Dong Ni; Ye, Chun Sheng; Zeng, Liang; Yin, Ping

doi:10.1177/000348941212100706

Cited by 14 publications

(7 citation statements)

References 24 publications

(41 reference statements)

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“…In particular, recent studies suggest the prognostic value of MTA1 in NPC because MTA1 overexpression was an independent prognostic factor for poor overall survival of NPC patients [8,9]. Our recent study provided direct evidence that MTA1 regulated actin cytoskeleton reorganization to promote NPC metastasis [7].…”

Section: Introductionmentioning

confidence: 73%

“…Only one report demonstrated that MTA1 overexpression was associated with larger tumor size in hepatocellular cancer [11]. Several studies examined the clinicopathological significance of MTA1 in NPC, but found no association between increased MTA1 expression and T-stage [8,9]. This may be due to the limitations of current T staging system of NPC for determining tumor burden [3].…”

Section: Discussionmentioning

confidence: 99%

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MTA1 promotes nasopharyngeal carcinoma growth in vitro and in vivo

Song

Zhang

Wang

et al. 2013

J Exp Clin Cancer Res

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BackgroundThe prognostic value of metastasis-associated gene 1 (MTA1) in nasopharyngeal carcinoma (NPC) has been suggested. However, there is still no direct evidence that MTA1 promotes NPC growth in vivo. In this study, we aimed to investigate the function of MTA1 in the regulation of NPC cell proliferation and tumorigenesis in vitro and in vivo.MethodsStable MTA1 knockdown or overexpression NPC cell lines were employed. The effects of MTA1 depletion or overexpression on cell proliferation, colony formation, cell cycle progression were examined by MTT, colony formation and flow cytometry assay. The effects of MTA1 depletion on tumor growth in vivo were examined in mouse xenograft model.ResultsMTA1 knockdown or overexpression drastically changed the proliferation, colony formation and cell cycle of NPC cells in vitro. MTA1 depletion significantly suppressed NPC tumorigenesis in vivo.ConclusionMTA1 promotes NPC cell proliferation via enhancing G1 to S phase transition, leading to increased tumor growth. Targeting MTA1 is a promising approach to reduce tumor burden of NPC.

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Section: Introductionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

MTA1 promotes nasopharyngeal carcinoma growth in vitro and in vivo

Song

Zhang

Wang

et al. 2013

J Exp Clin Cancer Res

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“…At this point, the upregulation of MTA1 has been detected in most malignant cancers in comparison with their normal tissue counterparts, including breast cancer [2,3,42,43], colorectal cancer [44][45][46], gastric cancer [44,47,48], esophageal carcinoma [49][50][51][52], pancreatic cancer [53,54], hepatocellular carcinoma [15,55,56], thymoma [57], lung cancer [58,59], osteosarcoma [16,60], endometrial adenocarcinoma [17], head and neck squamous cell carcinoma [61], oral squamous cell carcinomas [62], ovarian cancer [63,64], prostate cancer [65,66], nasopharyngeal carcinoma [67,68], cervical cancer [69], chorionic carcinoma [70], and B cell lymphomas [71,72]. The upregulation of MTA1 expression contributes to cell transformation, the epithelial-mesenchymal transition (EMT), cell proliferation, anchorageindependent cell growth, cell metastatic ability, angiogenesis, survival, and drug resistance.…”

Section: The Expression and Roles Of Mta1 In Malignant Tumorsmentioning

confidence: 99%

Subcellular localization of MTA proteins in normal and cancer cells

Liu

Wang

Huang

et al. 2014

Cancer Metastasis Rev

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The subcellular localization of a protein is closely linked to and indicates its function. The metastatic tumor antigen (MTA) family has been under continuous investigation since its identification two decades ago. MTA1, MTA2, and MTA3 are the main members of the MTA family. MTA1, as the representative member of this family, has been shown to be widely expressed in both embryonic and adult tissues, as well as in normal and cancerous conditions, indicating that MTA1 has functions both in physiological and pathological contexts. MTA1 is expressed at a higher level in most cancers than in their normal tissue counterparts. Even in normal cells, MTA1 levels vary a great deal from tissue to tissue. Importantly, MTA1 shows a multiple localization pattern in the cell, as do MTA2 and MTA3. Different MTA components in different subcellular compartments may exert different molecular functions in the cell. Previous studies revealed that MTA1 and MTA2 are predominately localized to the nucleus, while MTA3 is observed in both the nucleus and cytoplasm. Recent studies have reported that MTA1 is located in the nucleus, cytoplasm, and the nuclear envelope. In the nucleus, MTA1 dynamically interacts with chromatin in a MTA1-K532 methylation-dependent manner, whereas cytoplasmic MTA1 binds to the microtubule skeleton. MTA1 also shows a dynamic distribution during the cell cycle. Further investigations are needed to identify the exact subcellular localizations of MTA proteins. We review the sub-cellular localization patterns of the MTA family members and give a comprehensive overview of their respective molecular activities in multiple contexts.

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“…The re-expression of TNS1 has been shown to promote the formation of focal adhesions and to decrease the migration and invasion of MDA-MB-231 human breast cancer cells (25). Reversion-inducing-cysteine-rich protein with kazal motifs (RECK) is a cysteine-rich, extracellular protein with protease inhibitor-like domains whose expression is significantly suppressed in several tumors (26), including NPC (27). RECK has been reported to inhibit tumor angiogenesis, invasion and metastasis by negatively regulating matrix metalloproteinases (MMPs) (28).…”

Section: Discussionmentioning

confidence: 99%

DLC-1, a candidate tumor suppressor gene, inhibits the proliferation, migration and tumorigenicity of human nasopharyngeal carcinoma cells

Feng¹,

Liu³

et al. 2013

International Journal of Oncology

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In our previous study we demonstrated the downregulation or loss of deleted in liver cancer‑1 (DLC-1) gene expression in nasopharyngeal carcinoma (NPC). In this study, we report the effects of the DLC-1 gene on NPC cells and its mechanisms of action. DLC-1 expression was restored in the 5-8F NPC cell line, which lacks DLC-1 expression, and the biological characteristics of 5-8F-DLC‑1 cells were analyzed by MTT assay, colony formation assay, flow cytometry (FCM), tumorigenesis analysis in nude mice, as well as invasion and migration assay. Differentially expressed genes in response to DLC-1 expression were screened using microarray analysis and identified by RT-PCR. The re-expression of DLC-1 in the NPC cells attenuated the proliferation and colony formation ability of the cells in vitro, blocked NPC cells at the G0/G1 phase, reduced tumorigenicity potential in vivo, inhibited the invasion and migration ability of NPC cells and resulted in the reorganization of the actin cytoskeleton. DLC-1 altered the gene expression profile in 5-8F cells. Some tumor suppressor genes (TSGs) were upregulated and some oncogenes were downregulated. These results demonstrate that DLC-1 gene can partially reverse the malignant phenotype of NPC cells by changing the tumor-related gene expression profile, and may be a candidate tumor suppressor gene and a promising diagnostic and therapeutic target in NPC.

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Aberrant Expression Levels of MTA1 and RECK in Nasopharyngeal Carcinoma: Association with Metastasis, Recurrence, and Prognosis

Abstract: The conversely abnormal expression levels of MTA1 and RECK may be collectively involved in progression of malignancies and may serve as molecular predictors for metastasis, recurrence, and prognosis of NPC.

Cited by 14 publications

References 24 publications

MTA1 promotes nasopharyngeal carcinoma growth in vitro and in vivo

MTA1 promotes nasopharyngeal carcinoma growth in vitro and in vivo

Subcellular localization of MTA proteins in normal and cancer cells

DLC-1, a candidate tumor suppressor gene, inhibits the proliferation, migration and tumorigenicity of human nasopharyngeal carcinoma cells

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