What does this research mean for the field?

Targeting the 4EBP1/HSP90β/Nrf2 axis sensitizes β-catenin-mutant hepatocellular carcinoma to mTOR inhibitors by inducing ferroptosis. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research aims to understand why β-catenin-mutant hepatocellular carcinoma resists mTOR inhibitors and to explore combination therapies.

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June 18, 2026Open Access

Targeting the 4EBP1/HSP90β/Nrf2 Axis Sensitizes β-catenin-mutant Hepatocellular Carcinoma to mTOR Inhibitors via Ferroptosis Induction

Key Points

This research aims to understand why β-catenin-mutant hepatocellular carcinoma resists mTOR inhibitors and to explore combination therapies.
Investigated mTOR pathway interactions in β-catenin-mutant HCC.
Evaluated multidrug combinations to enhance the effect of mTOR inhibitors.
β-catenin mutations were linked to mTOR inhibitor resistance.
Combination therapies showed improved outcomes in β-catenin-mutant HCC.

Abstract

The aberrant activation of the mTOR pathway and its crosstalk with other signaling cascades represent key drivers of hepatocellular carcinoma (HCC) progression. mTOR-mediated ferroptosis suppression has been implicated in HCC resistance to chemotherapy. This study aimed to elucidate the mechanisms underlying mTOR inhibitor resistance and to evaluate the therapeutic potential of multidrug combinations in β-catenin-mutant HCC.

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