---
title: "ERα-driven m6A reader HNRNPC stabilizes DDX6 mRNA and promotes progression in ER+ breast cancer"
id: "british-journal-of-cancer-2-era-induced-m-6-a-reader-hnrnpc-maintains-ddx6-mrna-stability-to-promote-tumor"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-2-era-induced-m-6-a-reader-hnrnpc-maintains-ddx6-mrna-stability-to-promote-tumor"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03506-x"
published_at: "2026-09-24T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# ERα-driven m6A reader HNRNPC stabilizes DDX6 mRNA and promotes progression in ER+ breast cancer
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-2-era-induced-m-6-a-reader-hnrnpc-maintains-ddx6-mrna-stability-to-promote-tumor
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03506-x)
- **Published At:** 2026-09-24T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The study identifies upregulation of the m6A reader **HNRNPC** in breast cancer, particularly in ER+ subtypes, and links this to tumor progression. - Knockdown of HNRNPC reduces breast cancer cell proliferation and metastasis in vitro and suppresses tumor growth in xenograft models, indicating an oncogenic role. - Mechanistically, HNRNPC binds the continuous uridine-rich region in the 3′UTR of **m6A-modified DDX6** mRNA in the nucleus and maintains **DDX6** mRNA stability in an m6A-dependent manner. - Estrogen receptor alpha (**ERα**) acts as a transcription factor that binds the **HNRNPC** promoter and transcriptionally upregulates HNRNPC expression, forming an **ERα/HNRNPC/DDX6** regulatory axis in ER+ breast cancer. - **DDX6**, an RNA helicase localized to P-bodies and stress granules, has been implicated as an oncogene in other cancers; here it is presented as a downstream effector stabilized by HNRNPC in BC. - Experimental approaches reported include RT-qPCR, western blot, RIP, meRIP, ChIP, RNA pull-down, RIP-Seq, transcriptomics analysis, and xenograft models; specific reagents, instruments, and primer lists are referenced in supplementary materials. - Human sample collection: six paired invasive breast carcinoma and adjacent tissues were obtained with informed consent from Wuhan Union Hospital (HUST); study approved by HUST Ethics Committee. - Cell lines used include ER+ breast cancer cell lines MCF7 and T47D and non-tumorigenic MCF-10A; culture conditions for MCF7 and T47D are described. - The report emphasizes readers as crucial m6A regulators determining RNA fate and notes prior examples (IGF2BP3, YTHDF1/2) while positioning HNRNPC as an m6A-structure-sensitive reader whose interaction can be modulated by m6A-induced RNA structural changes. - Where the full experimental datasets, quantitative results, and some procedural details are not included in the provided source excerpt, those specifics were not reported in the source text available here.
## Clinical Analysis & Structured Key Points
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[articles](https://www.nature.com/bjc/articles?type=article) 4. article ERa-induced m6A reader HNRNPC maintains DDX6 mRNA stability to promote tumor progression in ER+BC [ Download PDF ](https://www.nature.com/articles/s41416-026-03506-x.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03506-x.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 24 September 2026 Molecular Diagnostics # ERa-induced m6A reader HNRNPC maintains DDX6 mRNA stability to promote tumor progression in ER+BC * [Ziwei Huang](https://www.nature.com/articles/s41416-026-03506-x#auth-Ziwei-Huang-Aff1)[1](https://www.nature.com/articles/s41416-026-03506-x#Aff1) [na1](https://www.nature.com/articles/s41416-026-03506-x#na1), * [Wenjie Xu](https://www.nature.com/articles/s41416-026-03506-x#auth-Wenjie-Xu-Aff2)[2](https://www.nature.com/articles/s41416-026-03506-x#Aff2) [na1](https://www.nature.com/articles/s41416-026-03506-x#na1), * [Yunxiao Xiao](https://www.nature.com/articles/s41416-026-03506-x#auth-Yunxiao-Xiao-Aff1)[1](https://www.nature.com/articles/s41416-026-03506-x#Aff1), * [Wenhui Li](https://www.nature.com/articles/s41416-026-03506-x#auth-Wenhui-Li-Aff1)[1](https://www.nature.com/articles/s41416-026-03506-x#Aff1), * [Ming Xu](https://www.nature.com/articles/s41416-026-03506-x#auth-Ming-Xu-Aff1)[1](https://www.nature.com/articles/s41416-026-03506-x#Aff1), * [Qiuyang Zhao](https://www.nature.com/articles/s41416-026-03506-x#auth-Qiuyang-Zhao-Aff1)[1](https://www.nature.com/articles/s41416-026-03506-x#Aff1) & * … * [Pengfei Yi](https://www.nature.com/articles/s41416-026-03506-x#auth-Pengfei-Yi-Aff1) [ORCID: orcid.org/0000-0003-1655-9696](https://orcid.org/0000-0003-1655-9696)[1](https://www.nature.com/articles/s41416-026-03506-x#Aff1) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03506-x#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03506-x/save-research?_csrf=upN-1Qq_K5nydSWCcvLB6NRd3Moull1-) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background Breast cancer (BC) remains a major threat to women’s health globally. The RNA m6A modification and its readers, such as heterogeneous nuclear ribonucleoprotein C (HNRNPC), which is upregulated in multiple cancers, play critical roles in tumorigenesis. ### Methods We assessed gene/protein expression (RT-qPCR, western blot) and cellular functions. Molecular mechanisms involving HNRNPC, DDX6, and m6A modifications were deciphered using RIP, meRIP, ChIP, and RNA pull-down assays. The oncogenic role of HNRNPC was confirmed in xenograft models. ### Results We found that HNRNPC has an abnormally high expression in BC, and knocking down HNRNPC could inhibit the tumor progression of BC. RNA immunoprecipitation revealed that HNRNPC could recognize and bind to the continuous “U” region in 3’UTR of m6A-modified DEAD-Box helicase 6 (DDX6) in the nucleus, which maintains the stability of DDX6 mRNA. Besides, estrogen receptor (ER) α could serve as a transcription factor and bind to the promoter site of HNRNPC, which up-regulated HNRNPC expression. ### Discussion We unveiled an ERα/HNRNPC/DDX6 axis in ER+ breast cancer, wherein ERα transcriptionally upregulates HNRNPC, which in turn stabilizes DDX6 mRNA in an m6A-dependent manner to drive tumor progression, suggesting HNRNPC as a promising therapeutic target. ### Similar content being viewed by others ![](https://media.springernature.com/w215h120/springer-static/image/art%3A10.1038%2Fs41419-022-05376-6/MediaObjects/41419_2022_5376_Fig1_HTML.png) ### [HNRNPU promotes the progression of triple-negative breast cancer via RNA transcription and alternative splicing mechanisms ](https://www.nature.com/articles/s41419-022-05376-6?fromPaywallRec=false) Article Open access 08 November 2022 ![](https://media.springernature.com/w215h120/springer-static/image/art%3A10.1038%2Fs41556-023-01141-9/MediaObjects/41556_2023_1141_Fig1_HTML.png) ### [An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus ](https://www.nature.com/articles/s41556-023-01141-9?fromPaywallRec=false) Article Open access 08 May 2023 ![](https://media.springernature.com/w215h120/springer-static/image/art%3A10.1038%2Fs41467-022-32537-0/MediaObjects/41467_2022_32537_Fig1_HTML.png) ### [HnRNPK maintains single strand RNA through controlling double-strand RNA in mammalian cells ](https://www.nature.com/articles/s41467-022-32537-0?fromPaywallRec=false) Article Open access 29 August 2022 ### Explore related subjects Discover the latest articles and news in related subjects. * [Breast cancer](https://www.nature.com/subjects/breast-cancer) * [Cancer](https://www.nature.com/subjects/cancer) ## Introduction Breast cancer (BC) is a growing threat to women’s health worldwide, having surpassed lung cancer in terms of morbidity globally in 2020 [[1](https://www.nature.com/articles/s41416-026-03506-x#ref-CR1 "Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, et al. Global Cancer Statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 Countries. CA Cancer J Clin. 2021;71:209–49.")]. In the United States alone, it is established that 287,850 new cases of BC will be diagnosed in the United States in 2022, and 43,250 patients succumbing to the disease [[2](https://www.nature.com/articles/s41416-026-03506-x#ref-CR2 "Giaquinto AN, Sung H, Miller KD, Kramer JL, Newman LA, Minihan A, et al. BC Statistics, 2022. CA Cancer J Clin. 2022;72:524–41.")]. With the development of molecular biology and sequencing technology, the molecular classification of BC has been established. Patients with localized tumors have a 5-year survival rate exceeding 90%, while those with advanced metastatic BC have a less than 30% 5-year survival rate [[2](https://www.nature.com/articles/s41416-026-03506-x#ref-CR2 "Giaquinto AN, Sung H, Miller KD, Kramer JL, Newman LA, Minihan A, et al. BC Statistics, 2022. CA Cancer J Clin. 2022;72:524–41.")], largely due to chemotherapy tolerance and metastasis. The formation and progression of BC is a complex process subject to regulation by epigenetics, including DNA and histone modifications, chromatin remodeling and RNA methylation [[3](https://www.nature.com/articles/s41416-026-03506-x#ref-CR3 "Pasculli B, Barbano R, Parrella P. Epigenetics of BC: Biology and clinical implication in the era of precision medicine. Semin Cancer Biol. 2018;51:22–35.")]. N6-methyladenosine (m6A), a widely studied RNA methylation, is involved in regulating various crucial life processes [[4](https://www.nature.com/articles/s41416-026-03506-x#ref-CR4 "Huang H, Weng H, Chen J. m\(6\)A Modification in coding and non-coding RNAs: roles and therapeutic implications in cancer. Cancer Cell. 2020;37:270–88.")], including BC. However, there are still unknowns about the regulatory roles of m6A in BC. Studies focusing on m6A will provide a better understanding of the molecular mechanisms underlying BC progression and potentially reveal new therapeutic targets for advanced BC. m6A means the methylation of the adenosine base at the nitrogen-6 position, is the most prevalent modification in coding and non-coding RNAs [[5](https://www.nature.com/articles/s41416-026-03506-x#ref-CR5 "Dominissini D, Moshitch-Moshkovitz S, Schwartz S, Salmon-Divon M, Ungar L, Osenberg S, et al. Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq. Nature. 2012;485:201–6.")]. The regulators of m6A include writer proteins, eraser proteins and reader proteins. Writers are methyltransferase, including METTL3, METTL14, WTAP, et al. Erasers are represented by FTO and ALKHB5, which can remove m6A modification. Readers can recognize and bind to m6A-modified sequence and thereby regulate the metabolism of the RNA [[6](https://www.nature.com/articles/s41416-026-03506-x#ref-CR6 "Jiang X, Liu B, Nie Z, Duan L, Xiong Q, Jin Z, et al. The role of m6A modification in the biological functions and diseases. Signal Transduct Target Ther. 2021;6:74."), [7](https://www.nature.com/articles/s41416-026-03506-x#ref-CR7 "Roundtree IA, Evans ME, Pan T, He C. Dynamic RNA modifications in gene expression regulation. Cell. 2017;169:1187–200.")]. In BC, FTO has been reported to mediate m6A demethylation in the 3’UTR of BNIP3 mRNA, a tumor suppressor, inducing its degradation [[8](https://www.nature.com/articles/s41416-026-03506-x#ref-CR8 "Niu Y, Lin Z, Wan A, Chen H, Liang H, Sun L, et al. RNA N6-methyladenosine demethylase FTO promotes breast tumor progression through inhibiting BNIP3. Mol Cancer. 2019;18:46.")]. Additionally, METTL3 can promote the expression of HBXIP with m6A modification, leading to the proliferation of BC cells [[9](https://www.nature.com/articles/s41416-026-03506-x#ref-CR9 "Cai X, Wang X, Cao C, Gao Y, Zhang S, Yang Z, et al. HBXIP-elevated methyltransferase METTL3 promotes the progression of BC via inhibiting tumor suppressor let-7g. Cancer Lett. 2018;415:11–9.")]. Readers are the most crucial regulators of m6A since they determine the fate of RNA. For example, IGF2BP3s maintain RNA stability [[10](https://www.nature.com/articles/s41416-026-03506-x#ref-CR10 "Jiang T, He X, Zhao Z, Zhang X, Wang T, Jia L. RNA m6A reader IGF2BP3 promotes metastasis of triple-negative BC via SLIT2 repression. FASEB J. 2022;36:e22618.")], while YTHDF2 accelerates RNA decay [[11](https://www.nature.com/articles/s41416-026-03506-x#ref-CR11 "Einstein JM, Perelis M, Chaim IA, Meena JK, Nussbacher JK, Tankka AT, et al. Inhibition of YTHDF2 triggers proteotoxic cell death in MYC-driven BC. Mol Cell. 2021;81:3048–64.e9.")]. Reader YTHDF1 has been shown to activate mRNA translation in BC cells and promote tumor progression [[12](https://www.nature.com/articles/s41416-026-03506-x#ref-CR12 "Chen H, Yu Y, Yang M, Huang H, Ma S, Hu J, et al. YTHDF1 promotes BC progression by facilitating FOXM1 translation in an m6A-dependent manner. Cell Biosci. 2022;12:19.")]. However, the functions of every reader protein in BC progression remain unclear. The relationship between reader proteins with estrogen receptor (ER), which have been considered key to BC metastasis and drug resistance [[13](https://www.nature.com/articles/s41416-026-03506-x#ref-CR13 "Drago JZ, Formisano L, Juric D, Niemierko A, Servetto A, Wander SA, et al. FGFR1 amplification mediates endocrine resistance but retains TORC sensitivity in metastatic hormone Receptor-Positive \(HR\(+\)\) BC. Clin Cancer Res. 2019;25:6443–51.")], remains unknown. Heterogeneous Nuclear Ribonucleoprotein C (HNRNPC), is highly expressed in various types of tumor cells. Studies showed that HNRNPC affected the metabolism of dsRNA via alternative splicing [[14](https://www.nature.com/articles/s41416-026-03506-x#ref-CR14 "Sarbanes SL, Le Pen J, Rice CM. Friend and foe, HNRNPC takes on immunostimulatory RNAs in BC cells. EMBO J. 2018;37:e100923.")]. Knocking down HNRNPC significantly decelerated cell proliferation in ER + BC cells MCF7 and T47D [[15](https://www.nature.com/articles/s41416-026-03506-x#ref-CR15 "Wu Y, Zhao W, Liu Y, Tan X, Li X, Zou Q, et al. Function of HNRNPC in BC cells by controlling the dsRNA-induced interferon response. EMBO J. 2018;37:e99017.")]. Interestingly, it has been reported that the change of RNA structure via m6A modification influences the combination ability of HNRNPC and RNA [[16](https://www.nature.com/articles/s41416-026-03506-x#ref-CR16 "Liu N, Dai Q, Zheng G, He C, Parisien M, Pan T. N\(6\)-methyladenosine-dependent RNA structural switches regulate RNA-protein interactions. Nature. 2015;518:560–4.")]. These results suggest that recognition and binding between HNRNPC and m6A-modified RNA may depend on RNA structure and that HNRNPC promotes BC progression depending on ERα. DEAD-Box Helicase 6 (DDX6), is an RNA helicase located primarily in P-bodies and stress granules [[17](https://www.nature.com/articles/s41416-026-03506-x#ref-CR17 "Nonhoff U, Ralser M, Welzel F, Piccini I, Balzereit D, Yaspo ML, et al. Ataxin-2 interacts with the DEAD/H-box RNA helicase DDX6 and interferes with P-bodies and stress granules. Mol Biol Cell. 2007;18:1385–96."), [18](https://www.nature.com/articles/s41416-026-03506-x#ref-CR18 "Fuller-Pace FV. DEAD box RNA helicase functions in cancer. RNA Biol. 2013;10:121–32.")]. DDX6 is primarily reported as an oncogene in colorectal cancer and gastric cancer, where it regulates the post-transcriptional regulation and translation of HER2, FGFR2 and c-Myc in P-bodies [[19](https://www.nature.com/articles/s41416-026-03506-x#ref-CR19 "Tajirika T, Tokumaru Y, Taniguchi K, Sugito N, Matsuhashi N, Futamura M, et al. DEAD-box protein RNA-helicase DDX6 regulates the expression of HER2 and FGFR2 at the post-transcriptional step in gastric cancer cells. Int J Mol Sci. 2018;19:2005."), [20](https://www.nature.com/articles/s41416-026-03506-x#ref-CR20 "Taniguchi K, Iwatsuki A, Sugito N, Shinohara H, Kuranaga Y, Oshikawa Y, et al. Oncogene RNA helicase DDX6 promotes the process of c-Myc expression in gastric cancer cells. Mol Carcinog. 2018;57:579–89.")]. DDX6 was also found to be required in the S phase of the cell cycle. However, the mechanism remains unclear [[21](https://www.nature.com/articles/s41416-026-03506-x#ref-CR21 "Akao Y, Matsumoto K, Ohguchi K, Nakagawa Y, Yoshida H. Human DEAD-box/RNA unwindase rck/p54 contributes to maintenance of cell growth by affecting cell cycle in cultured cells. Int J Oncol. 2006;29:41–8.")]. In BC, few studies have been published regarding the function of DDX6 and it is unknown whether DDX6 is regulated by m6A modification. In this study, we focused on m6A readers in BC, finding that HNRNPC was aberrantly up-regulated. Transcriptomics analysis revealed that ERα played a positive role in promoting elevated HNRNPC expression. Moreover, we demonstrated that HNRNPC recognized and bound the m6A modification region of DDX6 mRNA via RIP-Seq, with HNRNPC maintaining DDX6 mRNA stability in a m6A-dependent manner. The ERα/HNRNPC/DDX6 axis facilitated BC proliferation and metastasis in vitro and in vivo. These findings provide a novel mechanism and potential therapeutic target for ER+ subtype BC patients. ## Methods and Materials ### RNA isolation and RT-qPCR Total RNA was extracted using TRIzol (Vazyme, Nanjing, China) reagent and then reverse-transcribed using HiScript II RT SuperMix for qPCR (Vazyme, Nanjing, China). qPCR was performed using AceQ qPCR SYBR Green Master Mix (Vazyme, Nanjing, China) on the quantitative real-time PCR instrument (Applied Biosystems, USA). GAPDH and U6 were used for the normalization of mRNA levels. The synthesis of primers involved in the study was accomplished by TSINGKE (TSINGKE, Beijing, China). Primer sequences are listed in Supplementary Table [1](https://www.nature.com/articles/s41416-026-03506-x#MOESM1). ### Protein extraction and western blotting Proteins were extracted from cells and tissues using RIPA lysis buffer (Beyotime Biotechnology, Wuhan, China) supplemented with PMSF, protease inhibitor, and phosphatase inhibitor. The extracted proteins were separated on SDS-PAGE gels and transferred to polyvinylidene difluoride (PVDF) membranes (Millipore, Merck, U.S.). The membranes were blocked in 5% skim milk for 2 h at room temperature and then incubated with specific primary antibodies overnight at 4 °C. Afterward, the membranes were washed with PBST for 3 times and incubated with secondary antibodies for 1.5 h at room temperature. Finally, all protein bands were visualized with PierceTM ECL Western Blotting Substrate (Thermo Fisher Scientific, Waltham, MA, USA) by ChemiDoc XRS+ (Bio-Rad Laboratories, Inc). The antibodies used in this study are listed in Suppl. Table [2](https://www.nature.com/articles/s41416-026-03506-x#MOESM1). ### Human samples In total, 6 paired invasive breast carcinoma (IBC) tissues and adjacent breast tissues were collected from patients who were diagnosed and had undergone surgery at Breast and Thyroid Surgery, Wuhan Union Hospital, Huazhong University of Science and Technology (HUST) after informed consent obtained. All tissues were confirmed by pathologists and then frozen in liquid nitrogen for preservation. This study was approved by the Ethics Committee of Human Research of HUST. ### Cell culture Human IBC cell lines (MCF7, T47D) and the normal breast epithelial cell line MCF-10A were purchased from ATCC. MCF7 cells were cultured in DMEM (Biological Industries, Israel) with 10% fetal bovine serum (FBS). T47D cells were cultured in RPMI-1640 (Biological Industries, Israel) with 10
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