Y-W Lin

National Defense Medical Center

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H.-C. LAI

National Defense Medical Center

Chih‐Peng Chang

National Cheng Kung University

Tang‐Yuan Chu

Tzu Chi University

M-H Yu

Tri-Service General Hospital

H-C Chou

National Health Research Institutes

PD Aplan

National Cancer Institute

Chung‐Hsin Chen

National Taiwan University Hospital

Jin‐Chuan Sheu

National Taiwan University Hospital

Guan‐Tarn Huang

China Medical University Hospital

P-H Su

National Defense Medical Center

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National Taiwan University Hospital

National Defense Medical Center

National Taiwan University

Tri-Service General Hospital

National Yang Ming Chiao Tung University

National Health Research Institutes

Genomics Research Center, Academia Sinica

Taipei Medical University

E-Da Hospital

Tzu Chi University

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A two-step protocol for the detection of rearrangements at the AZFc region on the human Y chromosome

Molecular Human Reproduction (2006)

Y-W Lin

The AZFc region on the human Y chromosome consists mainly of very long direct and inverted repeats and is prone to rearrangement. Although deletion of the entire AZFc is found only in subfertile men, duplications and deletions of portions of AZFc as well as inversions are quite common and represent major polymorphisms of the Y chromosome. Several methods are available to detect these rearrangements, and each has its own advantages and limits. We designed a two-step PCR protocol to study the polymorphic structure of AZFc. The first PCR determines the copy number of the Deleted in Azoospermia (DAZ) genes within AZFc using the autosomal DAZ-Like gene as a dosage control, and the results could be verified by dosage Southern blot analyses. The second PCR simultaneously detects five sequence tagged sites (STSs) that are either present or absent in the various AZFc partial deletions. One of the STSs, sY1291, was found to be polymorphic in size due to varying lengths of a poly-T stretch. A combination of the DAZ dosage PCR and the 5-STS multiplex PCR reaction detects most, if not all, deletions and duplications at AZFc. It offers a simple and reliable way to screen large populations for AZFc rearrangements and study their effects on male fertility.

Sequence-tagged site

10.1093/molehr/gal038

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Citations (24)

Gene expression profiling of precursor T-cell lymphoblastic leukemia/lymphoma identifies oncogenic pathways that are potential therapeutic targets

Leukemia (2007)

Y-W Lin PD Aplan

10.1038/sj.leu.2404685

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Epigenetic silencing of PTPRR activates MAPK signaling, promotes metastasis and serves as a biomarker of invasive cervical cancer

Oncogene (2012)

P-H Su Y-W Lin R-L Huang Y-P Liao H. Y. Lee

DNMT3B

10.1038/onc.2012.29

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NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial–mesenchymal transition

Oncogene (2015)

Li Hj P-N Yu Kuo‐Yen Huang H-Y Su T-H Hsiao

The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic β-cells and neurons. Although recent publications show that NKX6.1 is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both in vitro and in vivo. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.

10.1038/onc.2015.289

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Citations (35)

Loss of heterozygosity and microsatellite instability in hepatocellular carcinoma in Taiwan

British Journal of Cancer (1999)

Jin‐Chuan Sheu Y-W Lin H-C Chou Guan‐Tarn Huang Mei–Hsuan Lee

Elucidation of the basic genetic changes of human hepatocellular carcinoma is important for the understanding and treatment of this cancer. We used microsatellite polymorphism markers to study 30 cases of hepatocellular carcinoma (34 tumours) on all human chromosomes. DNA from 34 pairs of hepatocellular carcinomas and corresponding non-tumour parts was prepared. Loss of heterozygosity (LOH) and microsatellite instability on 23 chromosomes were investigated by 231 sets of microsatellite markers. More than 20% LOH was shown for loci on 16q (47.1%), 13q (32.4%), 17p (32.4%), 5q (26.5%), 11p (23.5%) and 9p (20.6%). The commonly affected regions were mapped to 16q12.1, 16q12.2, 16q24, 13q12.1–32, 17p13, 5q32, 5q34, 5q3, 11p15, 11q23–24 and 9p21. Hepatitis B virus carriers had a significantly higher frequency of LOH on chromosomes 5q, 11p and 16q. Furthermore, larger tumour size tended to have higher frequency of LOH at D16S409 locus (16q12.1). Microsatellte instability was only found in 12 of 231 markers and the frequency is very low. These data suggest that the chromosomes 16q, 13q, 17p, 5q, 11p and 9p might participate in hepatocarcinogenesis. However, microsatellite instability might play little role in the development of this cancer in Taiwan.

Microsatellite Instability

10.1038/sj.bjc.6690380

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Citations (66)