What does this research mean for the field?

CSTF2 promotes ER-positive breast cancer progression and glycolytic metabolic reprogramming by binding to m⁶A-modified ATAD2 mRNA, thereby enhancing its stability and translation. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine the molecular mechanism by which CSTF2 regulates ATAD2 expression and influences metabolic reprogramming and tumor progression in breast cancer.

September 5, 2026HereditasOpen Access

CSTF2 facilitates ATAD2 translation via m⁶A recognition to drive ER-positive breast cancer metabolic reprogramming and tumor progression

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Authors

YLYing LiangNingxia Hui Autonomous Region Peoples Hospital MZMiao ZhangNingxia Hui Autonomous Region Peoples Hospital DNDianbin NingHebei General Hospital

Discussion

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Overview

Preclinical study reveals that CSTF2 accelerates breast cancer progression by stabilizing ATAD2, highlighting the CSTF2/ATAD2 axis as a potential therapeutic target.

Key Points

To determine the molecular mechanism by which CSTF2 regulates ATAD2 expression and influences metabolic reprogramming and tumor progression in breast cancer.
Assessed CSTF2 and ATAD2 expression across public breast cancer databases and cell lines, evaluating proliferation, invasion, apoptosis, and energy metabolism (ECAR/OCR) in MCF-7 cells.
Identified downstream targets and verified CSTF2 binding to m⁶A-modified ATAD2 mRNA using RNA immunoprecipitation, actinomycin D mRNA stability assays, and polysome profiling.
Conducted in vitro rescue assays and established an in vivo xenograft mouse model to evaluate tumor growth and metabolic protein expression changes following CSTF2 and ATAD2 modulation.
CSTF2 was significantly upregulated in breast cancer, and its overexpression enhanced MCF-7 cell proliferation, migration, invasion, glucose uptake, and lactate production while reducing apoptosis.
CSTF2 bound directly to m⁶A-modified ATAD2 mRNA to enhance its stability and translation efficiency, driving increased expression of glycolytic markers (HK2, PKM2) and repression of oxidative phosphorylation markers (SDHB, COX IV).
ATAD2 knockdown fully reversed CSTF2-induced metabolic reprogramming and aggressive oncogenic phenotypes in vitro, as well as abrogating accelerated xenograft tumor growth in vivo.

Cite This Study

Liang et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4046b95aff0620eb3f1 https://doi.org/10.1186/s41065-026-00735-1

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September 5, 2026HereditasOpen Access

CSTF2 facilitates ATAD2 translation via m⁶A recognition to drive ER-positive breast cancer metabolic reprogramming and tumor progression

View Full Paper

Ask AI

Bookmark

Authors

YLYing LiangNingxia Hui Autonomous Region Peoples Hospital MZMiao ZhangNingxia Hui Autonomous Region Peoples Hospital DNDianbin NingHebei General Hospital

Discussion

Member takes

Overview

Preclinical study reveals that CSTF2 accelerates breast cancer progression by stabilizing ATAD2, highlighting the CSTF2/ATAD2 axis as a potential therapeutic target.

Key Points

To determine the molecular mechanism by which CSTF2 regulates ATAD2 expression and influences metabolic reprogramming and tumor progression in breast cancer.
Assessed CSTF2 and ATAD2 expression across public breast cancer databases and cell lines, evaluating proliferation, invasion, apoptosis, and energy metabolism (ECAR/OCR) in MCF-7 cells.
Identified downstream targets and verified CSTF2 binding to m⁶A-modified ATAD2 mRNA using RNA immunoprecipitation, actinomycin D mRNA stability assays, and polysome profiling.
Conducted in vitro rescue assays and established an in vivo xenograft mouse model to evaluate tumor growth and metabolic protein expression changes following CSTF2 and ATAD2 modulation.
CSTF2 was significantly upregulated in breast cancer, and its overexpression enhanced MCF-7 cell proliferation, migration, invasion, glucose uptake, and lactate production while reducing apoptosis.
CSTF2 bound directly to m⁶A-modified ATAD2 mRNA to enhance its stability and translation efficiency, driving increased expression of glycolytic markers (HK2, PKM2) and repression of oxidative phosphorylation markers (SDHB, COX IV).
ATAD2 knockdown fully reversed CSTF2-induced metabolic reprogramming and aggressive oncogenic phenotypes in vitro, as well as abrogating accelerated xenograft tumor growth in vivo.

Cite This Study

Liang et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4046b95aff0620eb3f1 https://doi.org/10.1186/s41065-026-00735-1

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