SNHG20/miR‑140‑5p/NDRG3 axis contributes to 5‑fluorouracil resistance in gastric cancer

Yu, Jie; Shen, Jie; Xu, Qiao; Cao, Longlei; Yang, Zhangling; Ye, Hui; Xi, Changlei; Zhou, Qichang; Wang, Peiyun; Gong, Zhigang

doi:10.3892/ol.2019.10439

Cited by 11 publications

(12 citation statements)

References 24 publications

(28 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NDRG3 is expressed ubiquitously, and in testes, NDRG3 is localized to the outer layers of seminiferous epithelium ( Zhao et al., 2001 ), suggesting that it could be involved in HR at damaged forks and during meiotic recombination in spermatogenesis. NDRG3 upregulation correlates with poor prognosis in prostate and liver cancer ( Lee et al., 2016 ) and has been linked to drug resistance ( Du et al., 2017 ; Yu et al., 2019 ), which could be linked to an HR function. Our results also suggest that mutations in the H2A ubiquitination machinery may promote resistance to ATM inhibitors and provide important insights relevant to ongoing clinical investigations of PLK1 inhibitors in cancer therapy ( Liu et al., 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination

et al. 2021

View full text Add to dashboard Cite

Summary Cells have evolved an elaborate DNA repair network to ensure complete and accurate DNA replication. Defects in these repair machineries can fuel genome instability and drive carcinogenesis while creating vulnerabilities that may be exploited in therapy. Here, we use nascent chromatin capture (NCC) proteomics to characterize the repair of replication-associated DNA double-strand breaks (DSBs) triggered by topoisomerase 1 (TOP1) inhibitors. We reveal profound changes in the fork proteome, including the chromatin environment and nuclear membrane interactions, and identify three classes of repair factors according to their enrichment at broken and/or stalled forks. ATM inhibition dramatically rewired the broken fork proteome, revealing that ataxia telangiectasia mutated (ATM) signalling stimulates DNA end resection, recruits PLK1, and concomitantly suppresses the canonical DSB ubiquitination response by preventing accumulation of RNF168 and BRCA1-A. This work and collection of replication fork proteomes provide a new framework to understand how cells orchestrate homologous recombination repair of replication-associated DSBs.

show abstract

Section: Discussionmentioning

confidence: 99%

Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In gastric cancer, it inhibits p21 expression (187), it can interact with miR140-5p to induce resistance to therapy (188), or it can sponge miR-495-3p in order to enhance cell proliferation (189). In ovarian cancer, SNHG20 can activate WNT/β-catenin signaling pathway, which promotes cell proliferation (190).…”

Section: Small Nucleolar Rna Host Gene 20 (Snhg20)mentioning

confidence: 99%

An Emerging Class of Long Non-coding RNA With Oncogenic Role Arises From the snoRNA Host Genes

et al. 2020

View full text Add to dashboard Cite

The small nucleolar RNA host genes (SNHGs) are a group of long non-coding RNAs, which are reported in many studies as being overexpressed in various cancers. With very few exceptions, the SNHGs (SNHG1, SNHG3, SNHG5, SNHG6, SNHG7, SNHG12, SNHG15, SNHG16, SNHG20) are recognized as inducing increased proliferation, cell cycle progression, invasion, and metastasis of cancer cells, which makes this class of transcripts a viable biomarker for cancer development and aggressiveness. Through our literature research, we also found that silencing of SNHGs through small interfering RNAs or short hairpin RNAs is very effective in both in vitro and in vivo experiments by lowering the aggressiveness of solid cancers. The knockdown of SNHG as a new cancer therapeutic option should be investigated more in the future.

show abstract

“…In addition to CRC, lncRNAs have fundamental roles in conferring resistance to 5-FU in other types of cancer, particularly gastric cancer and HCC. For instance, in gastric cancer cells, SNHG20 has been shown to mediate resistance to 5-FU via modulating the expression of miR-140-5p and subsequent upregulation of its target gene NDRG3 (138). The role of PVT1 in the progression of this kind of cancer and induction of chemoresistance is mediated via up-regulation of the antiapoptotic gene Bcl2 (139).…”

Section: Lncrnas and Response To 5-fumentioning

confidence: 99%

5-Fluorouracil: A Narrative Review on the Role of Regulatory Mechanisms in Driving Resistance to This Chemotherapeutic Agent

et al. 2021

View full text Add to dashboard Cite

5-fluorouracil (5-FU) is among the mostly administrated chemotherapeutic agents for a wide variety of neoplasms. Non-coding RNAs have a central impact on the determination of the response of patients to 5-FU. These transcripts via modulation of cancer-related pathways, cell apoptosis, autophagy, epithelial–mesenchymal transition, and other aspects of cell behavior can affect cell response to 5-FU. Modulation of expression levels of microRNAs or long non-coding RNAs may be a suitable approach to sensitize tumor cells to 5-FU treatment via modulating multiple biological signaling pathways such as Hippo/YAP, Wnt/β-catenin, Hedgehog, NF-kB, and Notch cascades. Moreover, there is an increasing interest in targeting these transcripts in various kinds of cancers that are treated by 5-FU. In the present article, we provide a review of the function of non-coding transcripts in the modulation of response of neoplastic cells to 5-FU.

show abstract

SNHG20/miR‑140‑5p/NDRG3 axis contributes to 5‑fluorouracil resistance in gastric cancer

Cited by 11 publications

References 24 publications

Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination

Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination

An Emerging Class of Long Non-coding RNA With Oncogenic Role Arises From the snoRNA Host Genes

5-Fluorouracil: A Narrative Review on the Role of Regulatory Mechanisms in Driving Resistance to This Chemotherapeutic Agent

Contact Info

Product

Resources

About