Dr Yuchen Feng

Dr Yuchen Feng

Post Doctoral Researcher

School of Medicine and Public Health

Career Summary

Biography

Yuchen Feng obtained a Bachelor degree in medicine from China in 2016 before moving to the University of Newcastle, Australia, where she obtained a PhD degree in medical biochemistry in 2021. During her PhD, she discovered, for the first time, the proto-oncoprotein c-Myc inactivates the tumor suppressor p53 in cancer cells through a pan-cancer upregulated long noncoding RNA MILIP, which drives cancer pathogenesis. This work was published in Nature Communications in 2020 with Yuchen Feng as a leading author. Moreover, this work was presented at both national and international conferences including an oral presentation in American Association for Cancer Research (AACR) Annual Meeting, and won several awards.

Dr Feng is currently a postdoctoral researcher at the University of Newcastle. Her research has focused on mechanisms of long noncoding RNAs in cancer and extended these investigations to potential clinical applications such as exploring lncRNAs as diagnostic biomarkers and therapeutic targets. She is familiar with a wide range of advanced technologies including high-throughput RNA-sequencing, TCGA data analysis and proteomics, and has employed these knowledge to her research work.


Qualifications

  • Doctor of Philosophy, University of Newcastle
  • Bachelor of Medicine, China Medical University - China

Keywords

  • RNA therapy
  • cancer biology
  • long non-coding RNA

Languages

  • English (Fluent)
  • Mandarin (Mother)

Fields of Research

Code Description Percentage
321101 Cancer cell biology 50
321104 Cancer therapy (excl. chemotherapy and radiation therapy) 50

Professional Experience

UON Appointment

Title Organisation / Department
Post Doctoral Researcher University of Newcastle
School of Medicine and Public Health
Australia

Awards

Award

Year Award
2021 Best New Publication Award
School of Medicine and Public Health, The University of Newcastle
2020 HDR Publication Award 2020
Faculty of Health and Medicine, The University of Newcastle
2020 Best Oral Presentation
Australian Association of Chinese Biomedical Scientists
2018 Best Oral Presentation
Australian Association of Chinese Biomedical Scientists
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (7 outputs)

Year Citation Altmetrics Link
2021 Feng YC, Zhao XH, Teng L, Thorne RF, Jin L, Zhang XD, 'The pan-cancer lncRNA MILIP links c-Myc to p53 repression', Molecular and Cellular Oncology, 8 (2021)

We have recently identified the MYC proto-oncogene, bHLH transcription factor (MYC, best known as c-Myc)-responsive pan-cancer lncRNA c-Myc-Inducible Long noncoding RNA Inactivati... [more]

We have recently identified the MYC proto-oncogene, bHLH transcription factor (MYC, best known as c-Myc)-responsive pan-cancer lncRNA c-Myc-Inducible Long noncoding RNA Inactivating P53 (MILIP) as an oncogenic driver. Our studies show that MILIP facilitates tumor protein p53 (TP53, best known as p53) turnover by reducing its SUMOylation through suppressing tripartite-motif family-like 2 (TRIML2), thus promoting cell survival, proliferation, and tumorigenicity. MILIP may thus represent an anti-cancer target for counteracting the c-Myc axis.

DOI 10.1080/23723556.2020.1842714
Co-authors Rick Thorne, Lei Jin, Xu Zhang
2021 Teng L, Feng YC, Guo ST, Wang PL, Qi TF, Yue YM, et al., 'The pan-cancer lncRNA PLANE regulates an alternative splicing program to promote cancer pathogenesis.', Nat Commun, 12 3734 (2021)
DOI 10.1038/s41467-021-24099-4
Co-authors Rick Thorne, Xu Zhang, Lei Jin, Ting La, Yuanyuan Zhang
2020 Feng YC, Liu XY, Teng L, Ji Q, Wu Y, Li JM, et al., 'c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis', Nature Communications, 11 (2020) [C1]
DOI 10.1038/s41467-020-18735-8
Citations Scopus - 9Web of Science - 8
Co-authors Xu Zhang, Lei Jin, Muhammad Jamaluddin, Rodney Scott, Yuanyuan Zhang, Ting La, Rick Thorne
2020 La T, Jin L, Liu XY, Song ZH, Farrelly M, Feng YC, et al., 'Cylindromatosis is required for survival of a subset of melanoma cells.', Oncology Research, 28 385-398 (2020) [C1]
DOI 10.3727/096504020x15861709922491
Co-authors Xu Zhang, Yuanyuan Zhang, Ting La, Lei Jin, Rick Thorne
2019 Yari H, Jin L, Teng L, Wang Y, Wu Y, Liu GZ, et al., 'LncRNA REG1CP promotes tumorigenesis through an enhancer complex to recruit FANCJ helicase for REG3A transcription', NATURE COMMUNICATIONS, 10 (2019) [C1]
DOI 10.1038/s41467-019-13313-z
Citations Scopus - 15Web of Science - 16
Co-authors Rick Thorne, Ting La, Yuanyuan Zhang, Lei Jin, Xu Zhang, Rodney Scott
2018 La T, Liu GZ, Farrelly M, Cole N, Feng YC, Zhang YY, et al., 'A p53-responsive miRNA network promotes cancer cell quiescence', Cancer Research, 78 6666-6679 (2018) [C1]

Cancer cells in quiescence (G0 phase) are resistant to death, and re-entry of quiescent cancer cells into the cell-cycle plays an important role in cancer recurrence. Here we show... [more]

Cancer cells in quiescence (G0 phase) are resistant to death, and re-entry of quiescent cancer cells into the cell-cycle plays an important role in cancer recurrence. Here we show that two p53-responsive miRNAs utilize distinct but complementary mechanisms to promote cancer cell quiescence by facilitating stabilization of p27. Purified quiescent B16 mouse melanoma cells expressed higher levels of miRNA-27b-3p and miRNA-455-3p relative to their proliferating counterparts. Induction of quiescence resulted in increased levels of these miRNAs in diverse types of human cancer cell lines. Inhibition of miRNA-27b-3p or miRNA-455-3p reduced, whereas its overexpression increased, the proportion of quiescent cells in the population, indicating that these miRNAs promote cancer cell quiescence. Accordingly, cancer xenografts bearing miRNA-27b-3p or miRNA-455-3p mimics were retarded in growth. miRNA-27b-3p targeted cyclin-dependent kinase regulatory subunit 1 (CKS1B), leading to reduction in p27 polyubiquitination mediated by S-phase kinase-associated protein 2 (Skp2). miRNA-455-3p targeted CDK2-associated cullin domain 1 (CAC1), which enhanced CDK2-mediated phosphorylation of p27 necessary for its polyubiquitination. Of note, the gene encoding miRNA-27b-3p was embedded in the intron of the chromosome 9 open reading frame 3 gene that was transcriptionally activated by p53. Similarly, the host gene of miRNA-455-3p, collagen alpha-1 (XXVII) chain, was also a p53 transcriptional target. Collectively, our results identify miRNA-27b-3p and miRNA-455-3p as important regulators of cancer cell quiescence in response to p53 and suggest that manipulating miRNA-27b-3p and miRNA-455-3p may constitute novel therapeutic avenues for improving outcomes of cancer treatment. Significance: Two novel p53-responsive microRNAs whose distinct mechanisms of action both stabilize p27 to promote cell quiescence and may serve as therapeutic avenues for improving outcomes of cancer treatment.

DOI 10.1158/0008-5472.CAN-18-1886
Citations Scopus - 8Web of Science - 8
Co-authors Lei Jin, Yuanyuan Zhang, Xu Zhang, Rick Thorne, Ting La
2017 Wang JY, Liu GZ, Wilmott JS, La T, Feng YC, Yari H, et al., 'Skp2-mediated stabilization of MTH1 promotes survival of melanoma cells upon oxidative stress', Cancer Research, 77 6226-6239 (2017) [C1]

MTH1 helps prevent misincorporation of ROS-damaged dNTPs into genomic DNA; however, there is little understanding of how MTH1 itself is regulated. Here, we report that MTH1 is reg... [more]

MTH1 helps prevent misincorporation of ROS-damaged dNTPs into genomic DNA; however, there is little understanding of how MTH1 itself is regulated. Here, we report that MTH1 is regulated by polyubiquitination mediated by the E3 ligase Skp2. In melanoma cells, MTH1 was upregulated commonly mainly due to its improved stability caused by K63-linked polyubiquitination. Although Skp2 along with other components of the Skp1-Cullin-F-box (SCF) ubiquitin ligase complex was physically associated with MTH1, blocking the SCF function ablated MTH1 ubiquitination and expression. Conversely, overexpressing Skp2-elevated levels of MTH1 associated with an increase in its K63-linked ubiquitination. In melanoma cell lines and patient specimens, we observed a positive correlation of Skp2 and MTH1 expression. Mechanistic investigations showed that Skp2 limited DNA damage and apoptosis triggered by oxidative stress and that MAPK upregulated Skp2 and MTH1 to render cells more resistant to such stress. Collectively, our findings identify Skp2-mediated K63-linked polyubiquitination as a critical regulatory mechanism responsible for MTH1 upregulation in melanoma, with potential implications to target the MAPK/Skp2/MTH1 pathway to improve its treatment.

DOI 10.1158/0008-5472.CAN-17-1965
Citations Scopus - 29Web of Science - 28
Co-authors Lei Jin, Xu Zhang, Rick Thorne, Ting La
Show 4 more journal articles

Conference (11 outputs)

Year Citation Altmetrics Link
2020 Teng L, Feng YC, La T, Zhang YY, Zhao XH, Sokulsky L, et al., 'LncRNA PLANE regulates NCOR2 alternative splicing and promotes tumorigenesis', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
Co-authors Ting La, Lei Jin, Xu Zhang, Yuanyuan Zhang
2020 La T, Zhao XH, Zhang YY, Feng YC, Yan XG, Sokulsky L, et al., 'Visualization of endogenous p27 and Ki67 reveals an IDH3-mediated metabolic switch toward oxidative phosphorylation in quiescent cells', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
Co-authors Xu Zhang
2020 Zhao XH, La T, Feng YC, Zhang YY, Yan XG, Sokulsky L, et al., 'Targeting oxidative phosphorylation for cancer treatment in colorectal cancer', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
Co-authors Xu Zhang
2020 Feng YC, Zhang YY, La T, Tabatabaee H, Zhao X, Yan XG, et al., 'c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
Co-authors Xu Zhang
2019 La T, Farrelly M, Cole N, Carnell M, Feng YC, Yan XG, et al., 'Visualization of Endogenous p27 and Ki67 Reveals Oxidative Phosphorylation-Dependent Survival ofQuiescent Cells', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Co-authors Rick Thorne, Xu Zhang
2019 Zhang YY, Ben S, La T, Feng YC, Tabataba H, Zhang LS, et al., 'Regulatory Roles of the lncRNA OVAAL on Cancer Cell Survival and Cellular Senescence', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Citations Web of Science - 1
Co-authors Xu Zhang
2019 Feng YC, Liu XY, Teng L, Wu Y, Ji Q, Gao W, et al., 'MILIP is a Pan Cancer-Associated Long Noncoding RNA that Links MYC to Inactivation of p53', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Co-authors Xu Zhang, Rick Thorne
2018 Tabatabaee H, Yari H, Feng Y, Zhang YY, La T, Lei J, Zhang XD, 'The Role of Ion Channels in Melanoma', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Xu Zhang, Yuanyuan Zhang
2018 Feng Y, Zhang XD, Jin L, Zhang YY, Yari H, La T, Tabatabaee H, 'Oncogenic upregulation of the long noncoding RNA5', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Lei Jin, Xu Zhang, Yuanyuan Zhang
2018 Zhang YY, Yan XG, Farrelly M, Yari H, Feng Y, La T, et al., 'Long noncoding RNA OVAAL promotes melanoma cell proliferation through translational suppression of p27', CANCER RESEARCH, Chicago, IL (2018)
DOI 10.1158/1538-7445.AM2018-2451
Co-authors Xu Zhang, Ting La, Lei Jin
2017 Jin L, Tabatabaeehatambakhsh H, Jiang CC, Yan XG, Wang JY, Zhang YY, et al., 'ACTN4 stabilises RIPK1 to function as an oncogenic driver in melanoma', CANCER RESEARCH, Washington, DC (2017)
DOI 10.1158/1538-7445.AM2017-4462
Co-authors Chenchen Jiang, Xu Zhang, Lei Jin, Ting La
Show 8 more conferences
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Dr Yuchen Feng

Position

Post Doctoral Researcher
Melanoma Research Laboratory
School of Medicine and Public Health
College of Health, Medicine and Wellbeing

Contact Details

Email yuchen.feng@newcastle.edu.au
Phone (02) 49261343
Mobile 0414546659

Office

Room Life Sciences Building Room LS2-04
Building Life Sciences Building
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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