Evidence map›Paper›PMID 41405991›Full record

ArticleCell reports2026

Liprin-α1 enhances PHLDB3 oncogenic function in colorectal cancer via activation of mTORC2-AKT1 pathway.

Hyun Min Ko, Bo Cao, Li Li, Hee-Won Park, Shelya X Zeng, Hua Lu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Hyun Min KoDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
Bo CaoDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
Li LiLaboratory of Translational Cancer Research, Ochsner Clinic Foundation, 1516 Jefferson Highway, New Orleans, LA 70201, USA.
Hee-Won ParkDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: hpark1@tulane.edu.
Shelya X ZengDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: szeng@tulane.edu.
Hua LuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. Electronic address: hlu2@tulane.edu.

Funding

Digital Nanoplasmonic Quantification of Tumor-derived Extracellular Vesicles in Plasma MicrosamplesU01CA252965 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI HU, TONY Y., LU, HUA · 2020 to 2024
$3.0M
The Role of p53-R249S’s GOF in HCC developmentR01CA234605 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2019 to 2023
$1.8M
Validating p53 Ser46 crotonylation as a potential target for possible anti-cancer therapyR21CA272890 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2022 to 2023
$388k
Targeting GRP78 for p53 activation as anti-cancer therapyR21CA190775 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2015 to 2016
$360k
Role of TFIIS.h in regulation of p53 responsive apoptosis and tumor suppressionR21CA201889 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2016 to 2017
$360k
NCI NIH HHS R01 CA234605NCI NIH HHS R21 CA190775NCI NIH HHS R21 CA201889NCI NIH HHS R21 CA272890NCI NIH HHS U01 CA252965
6 · The paper itself

Abstract

Colorectal cancer (CRC) progression is driven by aberrant activation of oncogenic pathways, including AKT1, which requires mTORC2-mediated phosphorylation at Ser473. This study identifies PHLDB3 and Liprin-α1 as key regulators of RICTOR-dependent, mTORC2-mediated AKT1 signaling, independently of p53. PHLDB3 interacts with RICTOR to enhance AKT1 phosphorylation and promote tumor progression. In p53-null CRC cells, PHLDB3 knockdown reduces AKT1 activation, whereas PHLDB3 overexpression increases it. Liprin-α1 stabilizes PHLDB3 by limiting its proteasomal degradation, thereby maintaining mTORC2 activity. Liprin-α1 depletion lowers PHLDB3 levels and impairs AKT1 signaling, whereas Liprin-α1 overexpression boosts PHLDB3-mediated AKT1 activation and CRC cell proliferation. Importantly, the Liprin-α1-PHLDB3 axis depends on RICTOR, underscoring a hierarchical regulation essential for AKT1 activation. PHLDB3 is significantly overexpressed in CRC and is associated with poor prognosis. These findings reveal a Liprin-α1-PHLDB3-mTORC2-AKT1 signaling pathway important for CRC growth and present this pathway as a promising therapeutic target in CRC.

Indexed as

CarcinogenesisColorectal NeoplasmsMechanistic Target of Rapamycin Complex 2Proto-Oncogene Proteins c-aktAnimalsCell Line, TumorCell ProliferationHumansMiceMice, NudePhosphorylationRapamycin-Insensitive Companion of mTOR ProteinSignal TransductionAKT1 protein, humanMechanistic Target of Rapamycin Complex 2Proto-Oncogene Proteins c-aktRapamycin-Insensitive Companion of mTOR ProteinRICTOR protein, humanAKT1and CRCCP: CancerLiprin-α1mTORC2PHLDB3RICTOR

Identifiers

PMID41405991
PMCPMC12934055

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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.