The USP21/YY1/SNHG16 axis contributes to tumor proliferation, migration, and invasion of non-small-cell lung cancer

Xu, Pei; Xiao, Haibo; Yang, Qi; Hu, Rui; Jiang, Lingyong; Bi, Rui; Jiang, Xueyan; Wang, Lei; Mei, Ju; Ding, Fang; Huang, Jianbing

doi:10.1038/s12276-019-0356-6

Cited by 56 publications

(62 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chen et al reported that USP21 enhanced the metastatic and proliferative ability of bladder cancer by regulating EZH2 27 . Xu et al showed that the USP21/YY1/SNHG16 axis enhances the progression of NSCL 28 . A study by Liu et al found that lncRNA FGD5-AS1 regulates oral squamous cell carcinoma progression by interacting with the miR-520b/USP21 axis 29 .…”

Section: Discussionmentioning

confidence: 99%

Identification of hsa_circ_0039053 as an up-regulated and oncogenic circRNA in hepatocellular carcinoma via the miR-637-mediated USP21 activation

Yang¹,

Fang²,

Liu³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

Accumulating evidence indicated that circular RNAs (circRNAs) are crucial regulators in tumorigenesis of hepatocellular carcinoma (HCC), but it is still unclear how hsa_circ_0039053 causes HCC. Herein, hsa_circ_0039053 was upregulated in HCC tissues and cell lines. The upregulation of hsa_circ_0039053 was linked to the advanced clinical characteristics of patients. Downregulation of hsa_circ_0039053 decreased the invasion and proliferative ability of tumors in vitro and as well as tumor growth in vivo . Mechanically, hsa_circ_0039053 positively regulated USP21 expression through interacting with miR-637. Moreover, overexpression of USP21 or silencing of miR-637 restored the inhibitory impacts of hsa_circ_0039053 silencing on HCC progression. Collectively, our study confirmed that hsa_circ_0039053 could be regarded as a competing endogenous RNA (ceRNA) to positively modulate the expression of USP21 combining with miR-637, which provided a potential target in HCC treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of hsa_circ_0039053 as an up-regulated and oncogenic circRNA in hepatocellular carcinoma via the miR-637-mediated USP21 activation

Yang¹,

Fang²,

Liu³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

show abstract

“…We showed that USP21 is also amplified in prostate cancer CTCs. USP21 amplification can increase proliferation, migration, and invasion [ 64 ]. In non-small-cell lung cancer (NSCLC), USP21 amplification is highly prevalent and it is speculated that inhibition of USP21 might serve as a promising therapeutic approach in NSCLC [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Genomic Analysis of Localized High-Risk Prostate Cancer Circulating Tumor Cells at the Single-Cell Level

Rangel‐Pozzo

Liu

Wajnberg

et al. 2020

Cells

View full text Add to dashboard Cite

Accurate risk classification of men with localized high-risk prostate cancer directly affects treatment management decisions and patient outcomes. A wide range of risk assessments and classifications are available. However, each one has significant limitations to distinguish between indolent and aggressive prostate cancers. Circulating tumor cells (CTCs) may provide an alternate additional source, beyond tissue biopsies, to enable individual patient-specific clinical assessment, simply because CTCs can reveal both tumor-derived and germline-specific genetic information more precisely than that gained from a single diagnostic biopsy. In this study, we combined a filtration-based CTC isolation technology with prostate cancer CTC immunophenotyping to identify prostate cancer CTCs. Next, we performed 3-D telomere profiling prior to laser microdissection and single-cell whole-exome sequencing (WES) of 21 CTCs and 4 lymphocytes derived from 10 localized high-risk prostate cancer patient samples. Localized high-risk prostate cancer patient CTCs present a high number of telomere signals with lower signal intensities (short telomeres). To capture the genetic diversity/heterogeneity of high-risk prostate cancer CTCs, we carried out whole-exome sequencing. We identified 202,241 single nucleotide variants (SNVs) and 137,407 insertion-deletions (indels), where less than 10% of these genetic variations were within coding regions. The genetic variation (SNVs + indels) and copy number alteration (CNAs) profiles were highly heterogeneous and intra-patient CTC variation was observed. The pathway enrichment analysis showed the presence of genetic variation in nine telomere maintenance pathways (patients 3, 5, 6, and 7), including an important gene for telomere maintenance called telomeric repeat-binding factor 2 (TRF2). Using the PharmGKB database, we identified nine genetic variations associated with response to docetaxel. A total of 48 SNVs can affect drug response for 24 known cancer drugs. Gene Set Enrichment Analysis (GSEA) (patients 1, 3, 6, and 8) identified the presence of CNAs in 11 different pathways, including the DNA damage repair (DDR) pathway. In conclusion, single-cell approaches (WES and 3-D telomere profiling) showed to be useful in unmasking CTC heterogeneity. DDR pathway mutations have been well-established as a target pathway for cancer therapy. However, the frequent CNA amplifications found in localized high-risk patients may play critical roles in the therapeutic resistance in prostate cancer.

show abstract

“…22 These results suggest that YY1 might be a potential target for tumor progression. In lung cancer, Xu et al indicate that the USP21/YY1/ SNHG16 axis contributes to tumor proliferation, migration, and invasion of nonsmall-cell lung cancer 23 ; and Li et al reveal that YY1 accelerates angiogenesis and progression in lung cancer through enhancing long noncoding RNA MCM3AP-AS1 expression. 24 Our work indicates that YY1 is necessary for hypoxia-induced stemness of lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Transcription factor YY1 enhances the stemness of lung cancer cells by stabilizing hypoxia factor HIF‐1α under a hypoxic microenvironment

Huang

Zhou

Zhang

2020

Environmental Toxicology

View full text Add to dashboard Cite

The hypoxic microenvironment can facilitate the tumor progression, and transcription factor YY1 holds promoting effects in various tumors. This work aims to investigate whether YY1 is involved in hypoxia-induced stemness of lung cancer cells. We showed that hypoxic microenvironment induced the expression of HIF-1α and YY1, and the stemness of lung cancer cells, which was attenuated by YY1 knockdown. Additionally, we found that YY1 regulates the hypoxia-induced stemness in a HIF-1α-dependent manner, but independent on p53 expression. Further analysis revealed that YY1 physically interacted with HIF-1α protein and stabilized HIF-1α protein. Our work indicates a novel YY1/HIF-1α axis regulating the stemness of lung cancer cells.

show abstract

The USP21/YY1/SNHG16 axis contributes to tumor proliferation, migration, and invasion of non-small-cell lung cancer

Cited by 56 publications

References 55 publications

Identification of hsa_circ_0039053 as an up-regulated and oncogenic circRNA in hepatocellular carcinoma via the miR-637-mediated USP21 activation

Identification of hsa_circ_0039053 as an up-regulated and oncogenic circRNA in hepatocellular carcinoma via the miR-637-mediated USP21 activation

Genomic Analysis of Localized High-Risk Prostate Cancer Circulating Tumor Cells at the Single-Cell Level

Transcription factor YY1 enhances the stemness of lung cancer cells by stabilizing hypoxia factor HIF‐1α under a hypoxic microenvironment

Contact Info

Product

Resources

About