What type of study is this?

This is a Animal Study study (also classified as: In Vitro Study).

What question did this study set out to answer?

This research aims to elucidate the molecular mechanisms by which DDX3X facilitates adaptation to proteotoxic stress in multiple myeloma.

December 8, 2025Blood

DDX3X facilitates adaption to proteotoxic stress by regulating the translation of MAPKAPK2 and the stability of TMCO1 via stress granules in multiple myeloma

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Authors

ENEnqi Ni CSChunyan Sun

Discussion

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Overview

Findings reveal that DDX3X enhances cell survival by regulating translation and stress granules in multiple myeloma, implying potential therapeutic targets.

Key Points

This research aims to elucidate the molecular mechanisms by which DDX3X facilitates adaptation to proteotoxic stress in multiple myeloma.
Used thapsigargin to induce endoplasmic reticulum stress and trigger stress granule formation.
Conducted eCLIP-seq and RIP-qPCR assays to identify target transcripts of RNA-binding proteins.
Employed CRISPR/Cas9 and Tet-on shRNA-mediated knockdown to inhibit gene expression.
Performed cell viability assays using MTS and flow cytometry.
Utilized immunoprecipitation-Mass Spectrometry to identify protein-protein interactions.
DDX3X promotes the formation of stress granules in primary multiple myeloma cells under stress conditions.
DDX3X directly interacts with MAPKAPK2 mRNA, regulating its translation and affecting apoptosis through altered phosphorylation of Hsp27.
Inhibition of DDX3X enhances apoptosis in multiple myeloma cells, especially when combined with proteasome inhibitors.
DDX3X stabilizes TMCO1, recruiting it into stress granules, thus maintaining calcium homeostasis in the endoplasmic reticulum.
Knockdown of DDX3X showed enhanced anti-tumor efficacy in a xenograft model with increased UPR marker levels.

Cite This Study

Ni et al. (2025) studied this question.

synapsesocial.com/papers/69362f364fa91c937236d355 https://doi.org/10.1182/blood-2025-3944

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December 8, 2025Blood

DDX3X facilitates adaption to proteotoxic stress by regulating the translation of MAPKAPK2 and the stability of TMCO1 via stress granules in multiple myeloma

View Full Paper

Ask AI

Bookmark

Authors

ENEnqi Ni CSChunyan Sun

Discussion

Member takes

Overview

Findings reveal that DDX3X enhances cell survival by regulating translation and stress granules in multiple myeloma, implying potential therapeutic targets.

Key Points

This research aims to elucidate the molecular mechanisms by which DDX3X facilitates adaptation to proteotoxic stress in multiple myeloma.
Used thapsigargin to induce endoplasmic reticulum stress and trigger stress granule formation.
Conducted eCLIP-seq and RIP-qPCR assays to identify target transcripts of RNA-binding proteins.
Employed CRISPR/Cas9 and Tet-on shRNA-mediated knockdown to inhibit gene expression.
Performed cell viability assays using MTS and flow cytometry.
Utilized immunoprecipitation-Mass Spectrometry to identify protein-protein interactions.
DDX3X promotes the formation of stress granules in primary multiple myeloma cells under stress conditions.
DDX3X directly interacts with MAPKAPK2 mRNA, regulating its translation and affecting apoptosis through altered phosphorylation of Hsp27.
Inhibition of DDX3X enhances apoptosis in multiple myeloma cells, especially when combined with proteasome inhibitors.
DDX3X stabilizes TMCO1, recruiting it into stress granules, thus maintaining calcium homeostasis in the endoplasmic reticulum.
Knockdown of DDX3X showed enhanced anti-tumor efficacy in a xenograft model with increased UPR marker levels.

Cite This Study

Ni et al. (2025) studied this question.

synapsesocial.com/papers/69362f364fa91c937236d355 https://doi.org/10.1182/blood-2025-3944

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