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  • Open Access

    ARTICLE

    MicroRNA-382 inhibits the proliferation of mouse spermatogonia by targeting Kmt5a

    YI ZHENG#, PENGFEI ZHANG#, JINSHENG ZHU#, LINGKAI ZHANG, WENXIAN ZENG*

    BIOCELL, Vol.44, No.2, pp. 201-207, 2020, DOI:10.32604/biocell.2020.08770

    Abstract Spermatogenesis is a highly efficient and intricate process in the testis by which mature spermatozoa are produced daily to maintain lifelong male fertility. Essential to this process are spermatogonia capable of both proliferation and differentiation. Nevertheless, the underlying mechanisms for spermatogonial proliferation and differentiation remain poorly understood. MicroRNAs (miRNAs) are a category of non-coding small RNAs with regulatory functions by binding to the 3’ untranslated region (UTR) of the target mRNA. Previous studies have demonstrated that miRNAs are capable of modulating cell proliferation, differentiation and apoptosis, but the roles of individual miRNAs in spermatogonial fate… More >

  • Open Access

    ARTICLE

    Overexpression of PER3 Inhibits Self-Renewal Capability and Chemoresistance of Colorectal Cancer Stem-Like Cells via Inhibition of Notch and β-Catenin Signaling

    Feng Zhang*, Hong Sun, Sai Zhang, Xin Yang, Guogang Zhang*, Tao Su

    Oncology Research, Vol.25, No.5, pp. 709-719, 2017, DOI:10.3727/096504016X14772331883976

    Abstract PER3, a circadian clock gene, plays an important role in colorectal cancer, but its action and underlying mechanism in colorectal cancer stem-like cells (CSCs) remain unclear. In this study, the colorectal CSCs were enriched in colorectal HCT-116 sphere-forming cells, expressing lower levels of stem cell markers CD133, CD44, LGR5, and SOX2 compared with HCT-116 cells. A drug-resistant strain from HCT-116 was established. Western blot and qRT-PCR analysis showed that PER3 was downregulated in colorectal CSCs and drug-resistant HCT-116. Overexpression of PER3 could strengthen 5-FU-induced inhibitory effects on colorectal CSCs, but knockdown of PER3 decreased its… More >

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