• Title/Summary/Keyword: molecular evidence

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MCPH1 Protein Expression in Normal and Neoplastic Lung Tissues

  • Zhang, Ji;Wu, Xiao-Bin;Fan, Jian-Jun;Mai, Li;Cai, Wei;Li, Dan;Yuan, Cheng-Fu;Bu, You-Quan;Song, Fang-Zhou
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7295-7300
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    • 2013
  • Lung cancer is the most common cause of cancer-related death in the world. The main types are small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC), the latter including squamous cell carcinoma (SCC), adenocarcinoma and large cell carcinoma. NSCLCs account for about 80% of all lung cancer cases. Microcephalin (MCPH1), also called BRIT1 (BRCT-repeat inhibitor of hTERT expression), plays an important role in the maintenance of genomic stability. Recently, several studies have provided evidence that the expression of MCPH1 gene is decreased in several different types of human cancers. We evaluated the expression of protein MCPH1 in 188 lung cancer and 20 normal lung tissues by immunohistochemistry. Positive MCPH1 staining was found in all normal lung samples and only some cancerous tissues. MCPH1-positive cells were significantly lower in lung carcinoma compared with normal tissues. Furthermore, we firstly found that MCPH1 expression in lung adenocarcinoma is higher than its expression in squamous cell carcinoma. Change in MCPH1 protein expression may be associated with lung tumorigenesis and may be a useful biomarker for identification of pathological types of lung cancer.

Morphological, Cytological and Molecular Evidence for Intersubgeneric F1 Hybrid between Glycine max x G. tomentella (콩 Glycine max와 G. tomentella의 종간교잡으로부터 얻은 Fl식물체 검증을 위한 형태적 · 세포학적 · 분자유전학적 연구)

  • Choi, In-Soo;Kim, Yong-Chul
    • Journal of Life Science
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    • v.18 no.4
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    • pp.454-460
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    • 2008
  • This study was carried out to demonstrate morphological, cytological and molecular evidence for intersubgeneric $F_1$ hybrid between Glycine tomentella and G. max cv. ‘Baemkong’. Morphological features of $F_1$ plant for pistil and stamen, flower color and growth habit showed intermediate type between G. tomentella and G. max cv. ‘Baemkong’. Chromosome number of $F_1$ plant was 2n=39, which explained the evidence of $F_1$ hybrid between G. tomentella (2n=38) and G. max cv. ‘Baemkong’ (2n=40). Polyacrylamide isoelectric focusing pattern for esterase and peroxidase also showed that the $F_1$ plant was true $F_1$ hybrid between G. tomentella and G. max cv. ‘Baemkong’. From RAPD analysis, we identified that 62 primers showing bands in $F_1$ hybrid had both bands from G. tomentella and G. max cv. ‘Baemkong’, which suggested that this was true $F_1$ hybrid. Based on our results from morphological, cytological and molecular analyses, we suggest that the $F_1$ plant was true intersubgeneric hybrid between G. tomentella and G. max cv. ‘Baemkong’. Our results still remain us further study to recover fertility of $F_1$ hybrids. The occurrence of maternal and/or paternal inheritance in $F_1$ hybrid from intersubgeneric cross between G. tomentella and G. max cv. ‘Baemkong’ need to be explained.

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

  • Jiang, Qian;Li, Feng;Shi, Kejian;Yang, Yang;Xu, Caimin
    • BMB Reports
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    • v.45 no.3
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    • pp.194-199
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    • 2012
  • Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at $Ser^{308}$. We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at $Ser^{308}$ serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise.

Molecular gas properties under ICM pressure: A Case study of NGC4402

  • Hahn, You-Jin;Chung, Ae-Ree
    • The Bulletin of The Korean Astronomical Society
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    • v.37 no.1
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    • pp.41.1-41.1
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    • 2012
  • Interactions between the galactic interstellar medium (ISM) and the intra cluster medium (ICM) are believed to be one of the main processes affecting galaxy evolution in cluster environments. The aim of our research is to study the molecular gas properties of a galaxy under the ICM pressure in the cluster environment. It has been well known that cluster galaxies are deficient in atomic hydrogen gas (HI gas) compared to their field counterparts and now there is much evidence that low density ISM is being removed by ram pressure due to ICM wind. Meanwhile, no significant molecular gas deficiency of the cluster galaxy population has been found yet they show overall lower star formation rate than galaxies in the field, and it is still puzzling how the star formation could decrease without stripping of dense molecular gas. To address this issue, we probe the detailed molecular gas properties of NGC 4402, located near the cluster center, as part of a study of four spiral galaxies in the Virgo Cluster. NGC 4402 is well known undergoing ram pressure stripping with a truncated HI disk($D_{HI}/D_{opt}$ - 0.75 and only 36% of HI gas compare to field galaxies of a similar size) and a disturbed gas morphology. Comparing the high resolution 12CO and 13CO data of NGC 4402 from the Sub Millimeter Array (SMA) with existing other wavelength data, we probe the spatial distribution and a physical condition of molecular gas under strong ICM pressure. We discuss the star formation activity might have been altered and hence how the global color of NGC4402 would change in the future.

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Brain somatic mutations in MTOR leading to focal cortical dysplasia

  • Lim, Jae Seok;Lee, Jeong Ho
    • BMB Reports
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    • v.49 no.2
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    • pp.71-72
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    • 2016
  • Focal cortical dysplasia type II (FCDII) is a focal malformation of the developing cerebral cortex and the major cause of intractable epilepsy. However, since the molecular genetic etiology of FCD has remained enigmatic, the effective therapeutic target for this condition has remained poorly understood. Our recent study on FCD utilizing various deep sequencing platforms identified somatic mutations in MTOR (existing as low as 1% allelic frequency) only in the affected brain tissues. We observed that these mutations induced hyperactivation of the mTOR kinase. In addition, focal cortical expression of mutant MTOR using in utero electroporation in mice, recapitulated the neuropathological features of FCDII, such as migration defect, cytomegalic neuron and spontaneous seizures. Furthermore, seizures and dysmorphic neurons were rescued by the administration of mTOR inhibitor, rapamycin. This study provides the first evidence that brain somatic activating mutations in MTOR cause FCD, and suggests the potential drug target for intractable epilepsy in FCD patients.

Human Papillomavirus Type 16/18 Oncoproteins: Potential Therapeutic Targets in Non-smoking Associated Lung Cancer

  • Zhang, Er-Ying;Tang, Xu-Dong
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.11
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    • pp.5363-5369
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    • 2012
  • High-risk human papillomavirus (HPV) especially HPV-16 and HPV-18 types are speculated to be important risk factors in non-smoking associated lung cancer in Asia. Increasing evidence has demonstrated that HPV oncoproteins may contribute to lung tumorigenesis and cell transformation. Importantly, HPV 16/18 E6 and E7 oncoproteins can mediate expression of multiple target genes and proteins, such as p53/pRb, VEGF, HIF-$1{\alpha}$, cIAP-2, and hTERT, and contribute to cell proliferation, angiogenesis and cell immortalization through different signaling pathways in lung cancer. This article provides an overview of experiment data on HPV-associated lung cancer, describes the main targets on which HPV E6/E7 oncoproteins act, and further discusses the potential signaling pathways in which HPV E6/E7 oncoproteins are involved. In addition, we also raise questions regarding existing problems with the study of HPV-associated lung cancer.

Emerging roles of protein disulfide isomerase in cancer

  • Lee, Eunyoug;Lee, Do Hee
    • BMB Reports
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    • v.50 no.8
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    • pp.401-410
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    • 2017
  • The protein disulfide isomerase (PDI) family is a group of multifunctional endoplasmic reticulum (ER) enzymes that mediate the formation of disulfide bonds, catalyze the cysteine-based redox reactions and assist the quality control of client proteins. Recent structural and functional studies have demonstrated that PDI members not only play an essential role in the proteostasis in the ER but also exert diverse effects in numerous human disorders including cancer and neurodegenerative diseases. Increasing evidence suggests that PDI is actively involved in the proliferation, survival, and metastasis of several types of cancer cells. Although the molecular mechanism by which PDI contributes to tumorigenesis and metastasis remains to be understood, PDI is now emerging as a new therapeutic target for cancer treatment. In fact, several attempts have been made to develop PDI inhibitors as anti-cancer drugs. In this review, we discuss the properties and diverse functions of human PDI proteins and focus on recent findings regarding their roles in the state of diseases including cancer and neurodegeneration.

Activation of Dihaloalkanes by Thiol-dependent Mechanisms

  • Guengerich, F. Peter
    • BMB Reports
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    • v.36 no.1
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    • pp.20-27
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    • 2003
  • Dihaloalkanes constitute an important group of chemicals because of their widespread use in industry and agriculture and their potential for causing toxicity and cancer. Chronic toxic effects are considered to depend upon bioactivation, either by oxidation or thiol conjugation. Considerable evidence links genotoxicity and cancer with glutathione conjugations reactions, and some aspects of the mechanisms have been clarified with 1,2-dihaloalkanes and dihalomethanes. Recently the DNA repair protein $O^6$-alkylguanine transferase has been shown to produce cytotoxicity and genotoxicity by mans of a thiol-dependent process with similarities to the glutathione reactions.

Three new species of Polysiphonia sensu lato (Rhodophyta) based on the morphology and molecular evidence

  • Kim, Byeongseok;Kim, Myung Sook
    • ALGAE
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    • v.29 no.3
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    • pp.183-195
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    • 2014
  • There are recognized three new species of Polysiphonia sensu lato at a 10-20 m water depth from Jeju Island, Korea. We described the morphology of three new species and analyzed rbcL sequences to infer phylogenetic relationships among Polysiphonia sensu lato. Polysiphonia amplacapilli sp. nov. is characterized by an epiphytic, discoid holdfast, 5-7 pericentral cells, large trichoblasts, lateral branches connecting with trichoblasts, only slightly corticated in the basal parts, cut-off rhizoids and a spiral arrangement of tetrasporangia. Polysiphonia morroides sp. nov. is characterized by saxicolous, cut-off rhizoids, four pericentral cells, ecorticate, spiral arrangement of tetrasporangia, and it was collected at the fast-flowing water habitat in 20-25 m depth. Polysiphonia sabulosia sp. nov. is characterized by ecorticate, 5-6 pericentral cells, a single filamentous trichoblast, lateral branches connecting with the trichoblasts, cut-off rhizoids, and spiral arrangement of tetrasporangia, and is growing in the sandy locations. The phylogenetic analysis of rbcL sequences demonstrated that three new species are clearly distinguished from other species of Polysiphonia sensu lato.

The Inhibitory Effect of Pioglitazone on Agonist-dependent Vascular Contractility

  • Je, Hyun-Dong;Cha, Sung-Jae;Jeong, Ji-Hoon
    • Molecular & Cellular Toxicology
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    • v.4 no.1
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    • pp.72-77
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    • 2008
  • The present study was undertaken to determine whether pioglitazone treatment influences on the agonist-induced vascular smooth muscle contraction and, if so, to investigate the related mechanism. The measurement of isometric contractions using a computerized data acquisition system was combined with molecular experiments. Pioglitazone decreased Rho-kinase activating agonist-induced contraction but not phorbol ester-induced contraction suggesting the least involvement of $Ca^{2+}$-independent thin filament regulation of contractility. Furthermore, pioglitazone decreased thromboxane $A_2$ mimeticinduced phosphorylation of MYPT1 at Thr855, the newly-highlighted site, instead of Thr696. In conclusion, this study provides the evidence and possible related mechanism concerning the vasorelaxing effect of pioglitazone as an antihypertensive on the agonist-induced contraction in rat aortic rings regardless of endothelial function.