1.Advances of long noncoding RNA in primary liver cancer
Chinese Journal of Laboratory Medicine 2014;(9):665-668
LncRNAs( long noncoding RNAs ) can be defined as RNA transcrips longer than 200nt without protein coding capacity , which play vital roles in various aspects of gene expression regulation.Recent investigations showed aberrant expression of many lncRNAs in primary liver cancer , indicating their important roles in tumorigenesis and development of liver cancer.This review focuses on the biological functions of lncRNAs and their involvements in primary liver cancer.
2.Oral tuberculosis:A case report
Jiantang YANG ; Lingwan GU ; Tingyu REN ; Jian ZHANG
Journal of Practical Stomatology 2014;(6):875-876
Oral tuberculosis is one of oral infectious diseases and there are some difficulties in its diagnosis.This article describes a case of oral gingival tuberculosis for that the diagnosis had not been confirmed by biopsy.Local injection with streptomycin was undertaken.1 month after treatment the gingival lesion was improved.
3.Acetylated Histone Expressions of the Primary Hippocampal Neurons in Rats Reduced by siCBP Lentivirus.
Nali HOU ; Xiaofeng WU ; Lan REN ; Min GUO ; Yang BI ; Youxue LIU ; Jie CHEN ; Hongmei HAUNG ; Tingyu LI
Journal of Biomedical Engineering 2015;32(4):838-846
This study aims to construct the recombinant lentivirus vector containing specific small interfering RNA (siRNA) targeting rat CREB binding protein(CBP)gene and to identify its function of inhibiting the expressions of acetylated histone in primarily cultured hippocampal neurons. Firstly, we constructed four kinds of recombinant lentivirus siCBP. And then we used them to infect the primarily cultured hippocampal neurons, and performed real-time PCR, western blot respectively to detect the expressions of CBP. Afterwards, the most effective lentivirus siCBP was used to infect the primarily cultured hippocampal neurons, and then the HAT activity and protein expressions of acetylated histone Ac-H3, Ac-H4 of the neurons were examined. By using PCR, endonuclease cutting and gene sequencing, we confirmed that the target genes were correctly cloned in lentivirus vector. Besides, CBP mRNA and protein expressions in neurons were found to be with varying degrees of decreases after infections of the four kinds of lentivirus siCBP. Furthermore, the representative and most effective lentivirus GR806 could effectively inhibit the HAT activity and the protein expressions of Ac-H3, Ac-H4 in neurons. It provides the experimental basis for the subsequent application of siCBP to clarify the effects and corresponding molecular mechanism of the CBP-dependent histone acetylation on learning and memory function in hippocampus.
Acetylation
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Animals
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CREB-Binding Protein
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metabolism
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Genetic Vectors
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Hippocampus
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cytology
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Histones
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metabolism
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Lentivirus
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Memory
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Neurons
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metabolism
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Primary Cell Culture
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RNA, Messenger
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RNA, Small Interfering
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Rats
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Real-Time Polymerase Chain Reaction
4.NDFIP1 limits cellular TAZ accumulation via exosomal sorting to inhibit NSCLC proliferation.
Yirui CHENG ; Xin LU ; Fan LI ; Zhuo CHEN ; Yanshuang ZHANG ; Qing HAN ; Qingyu ZENG ; Tingyu WU ; Ziming LI ; Shun LU ; Cecilia WILLIAMS ; Weiliang XIA
Protein & Cell 2023;14(2):123-136
NDFIP1 has been previously reported as a tumor suppressor in multiple solid tumors, but the function of NDFIP1 in NSCLC and the underlying mechanism are still unknown. Besides, the WW domain containing proteins can be recognized by NDFIP1, resulted in the loading of the target proteins into exosomes. However, whether WW domain-containing transcription regulator 1 (WWTR1, also known as TAZ) can be packaged into exosomes by NDFIP1 and if so, whether the release of this oncogenic protein via exosomes has an effect on tumor development has not been investigated to any extent. Here, we first found that NDFIP1 was low expressed in NSCLC samples and cell lines, which is associated with shorter OS. Then, we confirmed the interaction between TAZ and NDFIP1, and the existence of TAZ in exosomes, which requires NDFIP1. Critically, knockout of NDFIP1 led to TAZ accumulation with no change in its mRNA level and degradation rate. And the cellular TAZ level could be altered by exosome secretion. Furthermore, NDFIP1 inhibited proliferation in vitro and in vivo, and silencing TAZ eliminated the increase of proliferation caused by NDFIP1 knockout. Moreover, TAZ was negatively correlated with NDFIP1 in subcutaneous xenograft model and clinical samples, and the serum exosomal TAZ level was lower in NSCLC patients. In summary, our data uncover a new tumor suppressor, NDFIP1 in NSCLC, and a new exosome-related regulatory mechanism of TAZ.
Humans
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Carcinoma, Non-Small-Cell Lung/metabolism*
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Carrier Proteins/metabolism*
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Cell Line
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Cell Proliferation
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Exosomes/metabolism*
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Lung Neoplasms/genetics*
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Membrane Proteins/metabolism*
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Transcriptional Coactivator with PDZ-Binding Motif Proteins/metabolism*