Evidence map›Paper›PMID 34965300›Full record

ArticleCarcinogenesis2022

A Combination therapy using an mTOR inhibitor and Honokiol effectively induces autophagy through the modulation of AXL and Rubicon in renal cancer cells and restricts renal tumor growth following organ transplantation.

Akash Sabarwal, Johannes Wedel, Kaifeng Liu, David Zurakowski, Samik Chakraborty, Evelyn Flynn, David M Briscoe, Murugabaskar Balan, Soumitro Pal

Open access · greenAbstract read
In one paragraph

Article in Carcinogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Phytochemicals as promising agents in Axl-targeted cancer treatment.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  3. AXL signaling in cancer: from molecular insights to targeted therapies.Signal transduction and targeted therapy · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Akash SabarwalDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
Johannes WedelDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
Kaifeng LiuDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
David ZurakowskiDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.ORCID 0000-0003-3610-6942
Samik ChakrabortyDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
Evelyn FlynnDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
David M BriscoeDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
Murugabaskar BalanDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.
Soumitro PalDivision of Nephrology, Boston Children's Hospital, Boston, MA 02115, USA.ORCID 0000-0002-9177-6634
Boston Children's Hospital · US

Funding

Novel Role(s) of Nrf2 in the Growth of Post-Transplantation CancerR01CA193675 · NCI · BOSTON CHILDREN'S HOSPITAL · PI PAL, SOUMITRO · 2016 to 2020
$2.0M
Protective role of Honokiol in preventing c-Met-induced post-transplantation cancerR01CA222355 · NCI · BOSTON CHILDREN'S HOSPITAL · PI PAL, SOUMITRO · 2018 to 2022
$2.0M
NCI NIH HHS R01 CA193675NCI NIH HHS R01 CA222355
6 · The paper itself

Abstract

Development of cancer, including renal cancer, is a major problem in immunosuppressed patients. The mTOR inhibitor Rapamycin (RAPA) is used as an immunosuppressive agent in patients with organ transplants and other immunological disorders; and it also has antitumorigenic potential. However, long-term use of RAPA causes reactivation of Akt, and ultimately leads to enhanced tumor growth. Honokiol (HNK) is a natural compound, which possesses both anti-inflammatory and antitumorigenic properties. In this study, we investigated the effect of a novel combination therapy using RAPA + HNK on allograft survival and post-transplantation renal tumor growth. We observed that it effectively modulated the expression of some key regulatory molecules (like Carabin, an endogenous Ras inhibitor; and Rubicon, a negative regulator of autophagy) that play important roles in tumor cell growth and survival. This combination induced toxic autophagy and apoptosis to promote cancer cell death; and was associated with a reduced expression of the tumor-promoting receptor tyrosine kinase AXL. Finally, we utilized a novel murine model to examine the effect of RAPA + HNK on post-transplantation renal tumor growth. The combination treatment prolonged the allograft survival and significantly inhibited post-transplantation tumor growth. It was associated with reduced tumor expression of Rubicon and the cytoprotective/antioxidant heme oxygenase-1 to overcome therapeutic resistance. It also downregulated the coinhibitory programmed death-1 ligand, which plays major role(s) in the immune escape of tumor cells. Together, this combination treatment has a great potential to restrict renal tumor growth in transplant recipients as well as other immunosuppressed patients.

Indexed as

Kidney NeoplasmsOrgan TransplantationAllyl CompoundsAnimalsApoptosisAutophagyBiphenyl CompoundsCell Line, TumorHumansIntracellular Signaling Peptides and ProteinsLignansMicePhenolsSirolimusTOR Serine-Threonine KinasesAllyl CompoundsBiphenyl CompoundshonokiolIntracellular Signaling Peptides and ProteinsLignansMTOR protein, humanPhenolsRubcn protein, mouseSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID34965300
PMCPMC9118982
OpenAlexW4205622233

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.