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Cited by 10Mechanisms of cancer metastasisCancer-related Molecular PathwaysBreast Cancer Treatment Studies

Rlip Depletion Suppresses Growth of Breast Cancer

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Bose, Chhanda, Yadav, Sushma, Singhal, Sharad S., Singhal, Jyotsana, Hindle, Ashly, Lee, Jihyun, Cheedella, Naga K. S., Rehman, Shabnam +7 more·2020·Cancers
DOI 10.3390/cancers12061446PMC PMC7352702
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Abstract

RLIP76 (RAL-binding protein-1, Rlip) is a stress-protective mercapturic-acid-pathway transporter protein that also plays a key role in regulating clathrin-dependent endocytosis as a Ral effector. Targeted inhibition or depletion of Rlip causes regression of xenografts of many cancers and is capable of abrogating tumor formation in p53-null mice. This is associated with the reversion of the abnormal methylomic profile of p53-null mice to wild-type. In a query of The Cancer Genome Atlas (TCGA) databases, we found that Rlip expression was associated with poor survival and with significant differences in the frequencies of PIK3CA mutation, MYC amplification, and CDKN2A/B deletion, which were the most commonly mutated, amplified, and deleted genes, respectively, among TCGA breast cancer patients. We conducted the present study to further examine the effects of Rlip inhibition and to evaluate the in vitro and in vivo efficacy in breast cancer. Using immunogold electron microscopy, we found that plasma-membrane Rlip was accessible to cell-surface antibodies in the MCF7 (ER+) breast cancer cell line. Rlip depletion resulted in decreased survival of MCF7 and MDA-MB-231 cells and increased terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positivity and DNA laddering, indicating apoptotic cell death. Additionally, in vitro knockdown of Rlip inhibited EGF endocytosis and WNT/MAPK signaling. Xenograft studies in nude mice showed regression of breast cancer via antisense-mediated depletion of Rlip mRNA as well as by anti-Rlip antibody. Finally, knockdown of Rlip by antisense locked nucleic acid oligonucleotides increased markers for apoptotic signaling and decreased markers for proliferation, angiogenesis, and cell cycling in MCF7 and MDA-MB-231luc xenografts. Our findings validate Rlip as an attractive target in breast cancer.

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Cited by

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Authors
Bose, C., Yadav, S., Singhal, S. S., Singhal, J., Hindle, A., Lee, J., Cheedella, N. K. S., Rehman, S., Layeequr Rahman, R., Jones, C., Darden, M., Palade, P. T., Berz, D., Singh, S. P., & Awasthi, S.
Affiliations
  • Texas Tech University (US)
  • City Of Hope National Medical Center (US)
  • Department of Internal Medicine, Division of Hematology & Oncology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA
  • University Medical Center Health System, UMC Cancer Center, Lubbock, TX 79415, USA
  • The University of Texas Health Science Center at Houston (US)
  • University of Arkansas for Medical Sciences (US)
  • Beverly Hills Cancer Center (US)
Corresponding author
  • Singh, Sharda P.
  • Awasthi, Sanjay
ORCID
Venue
Cancers
Publisher
MDPI AG
Published
2020-06-02
Volume
12
Issue
6
Pages
1446
ISSN
2072-6694 (ISSN-L)
DOI
10.3390/cancers12061446
PMC
PMC7352702
OpenAlex
W3033084644
Cited by
10
References
1
Citations by year
2026: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 4
FWCI
0.64
Type
journal article
Language
en
Open access
Licence
Locations
  • Cancers (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • U.S. Department of Defense (W81XWH-16, W81XWH, W81XWH-18)
  • Comprehensive Cancer Center, City of Hope
  • U.S. Public Health Service (CA107399)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
Keywords
RLIP76, breast cancer, clathrin-mediated endocytosis, apoptosis, p53-null mice, DNA methylation, PIK3CA mutation, MYC amplification, CDKN2A/B deletion, MCF-7 cells, MDA-MB-231 cells, therapeutic target

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