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Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity
Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity
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Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity
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Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity
Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity

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Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity
Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity
Journal Article

Identification of UAP1L1 as a critical factor for prostate cancer and underlying molecular mechanism in tumorigenicity

2022
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Overview
Background Prostate cancer is the second most common cancer in men, and some new target genes are needed to predict the risk of prostate cancer progression and the treatment. Methods In this study, the effects of UAP1L1 (UAP1-like-1) on prostate cancer were investigated by detecting the proliferation, migration, invasion and apoptosis of prostate cancer cells in vitro using MTT, wound healing, Transwell and flow cytometry assay, and the tumor growth in vivo. The downstream genes and pathways of UAP1L1 were explored using Ingenuity Pathway Analysis (IPA), and screened by qRT-PCR and western blot. The effects of CDCA8 on prostate cancer cells were also verified in vitro, which was through detecting the change of proliferation, migration, invasion and apoptosis of prostate cancer cells after CDCA8 knockdown. Results The results indicated that UAP1L1 promoted the proliferation, migration and invasion of prostate cancer cells, which was inhibited by downregulating CDCA8. Furthermore, the promotion of CDCA8 knockdown on cell apoptosis was reduced when UAP1L1 was simultaneously overexpressed. Conclusions In conclusion, the results in this study revealed that UAP1L1 promoted the progression of prostate cancer through the downstream gene CDCA8.