Targeting myeloid derived suppressor cells reverts immune suppression and sensitizes BRAF-mutant papillary thyroid cancer to MAPK inhibitors
Open accessAbstract
MAPK signaling inhibitor (MAPKi) therapies show limited efficacy for advanced thyroid cancers despite constitutive activation of the signaling correlates with disease recurrence and persistence. Understanding how BRAF pathway stimulates tumorigenesis could lead to new therapeutic targets. Here, through genetic and pathological approaches, we demonstrate that BRAF V600E promotes thyroid cancer development by increasing myeloid-derived suppressor cells (MDSCs) penetrance. This BRAF V600E-induced immune suppression involves re-activation of the developmental factor TBX3, which in turn up-regulates CXCR2 ligands in a TLR2-NFκB dependent manner, leading to MDSCs recruitment into the tumor microenvironment. CXCR2 inhibition or MDSCs repression improves MAPKi therapy effect. Clinically, high TBX3 expression correlates with BRAF V600E mutation and increased CXCR2 ligands, along with abundant MDSCs infiltration. Thus, our study uncovers a BRAF V600E-TBX3-CXCLs-MDSCs axis that guides patient stratification and could be targeted to improve the efficacy of MAPKi therapy in advanced thyroid cancer patients.
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Expression levels of USP15 and TBX3 are significantly increased and positively correlated with tumor progression in thyroid cancer tissue array samples.
“Across the 152 tissue array samples composed mainly of PTC samples with adjacent tissues, as well as a small number of other types of thyroid cancer tissues, expression levels of USP15 and TBX3 are significantly increased and positively correlated with tumor progression15 (Supplementary Fig. 4a).”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
The Results section reports that TBX3 was up-regulated and correlated with histological grade in 110 PTC specimens. It does not report USP15 expression or a 152-sample tissue array, so those parts of the attributed claim are unsupported by this paper. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPathologically activated BRAF/MAPK signaling, possibly by BRAFV600E, initiates and promotes tumor development through transcriptionally elevating USP15 and protecting TBX3 from degradation, in addition to directly transcriptionally up-regulating TBX3.
“Therefore, pathologically activated BRAF/MAPK signaling, possibly by BRAFV600E, initiates and promotes tumor development through transcriptionally elevating USP15 and protecting TBX3 from degradation, in addition to direct transcriptionally up-regulating TBX315.”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredUpregulation of pioneer developmental organizers such as SOX2, KLF4, β-catenin, SNAIL-1, c-MYC, TBX3, and BCL6 is reported downstream of BRAF/MAPK-driven tumor.
“Even upregulation of pioneer developmental organizers, such as SOX2, KLF4, β-catenin, SNAIL-1, c-MYC, TBX3, BCL6, et al., are reported downstream of BRAF/MAPK-driven tumor, the pathways causing lineage reprogramming are not clear12,15,30–36.”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
The Results section, “BRAF/MAPK directs TBX3 expression through AP-1-mediated transcriptional regulation” (page unavailable), reports that BRAF/MAPK activity increases TBX3 expression in papillary thyroid cancer cells. The cited paper supports TBX3 as an example, but the passages do not establish BRAF/MAPK-driven upregulation of the other listed factors. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTbx3 knockout restores differentiation factor expression and renders re-differentiation marked by Tpo, Nis, Tg in BRAFV600E-driven tumors.
“Tbx3 knockout restored differentiation factors expression and rendered re-differentiation marked with, but not limited to Tpo, Nis, Tg15 (Fig. 7a).”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
The Discussion says Tbx3 ablation ameliorates the BRAFV600E-associated reduction of thyroid lineage factors, supporting the general differentiation-factor claim. Our copy does not identify Tpo, Nis, and Tg as markers restored by knockout, and the Results report no significant relief of lineage-factor expression after later postnatal Tbx3 knockout. (LLM, conf=0.85)
Experimental — accuracy not yet measuredBRAF/MAPK pathway up-regulates developmental factor TBX3 for tumorigenesis by interfering with the proteostasis module in addition to transcriptional regulation.
“Therefore, BRAF/MAPK pathway up-regulates developmental factor TBX3 for tumorigenesis by interfering with the proteostasis module in addition to transcriptional regulation15”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
The Results section, “BRAF/MAPK directs TBX3 expression through AP-1-mediated transcriptional regulation” (page unavailable), supports BRAF/MAPK-driven TBX3 up-regulation through AP-1 transcriptional activation. The Discussion links TBX3 activation to thyroid tumor initiation. Neither passage supports the additional claim that BRAF/MAPK interferes with a proteostasis module to up-regulate TBX3. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Multiple oncogenic pathways regulate TBX3 expression in melanoma, lung, thyroid, breast and other cancers.
“Multiple oncogenic pathways have been found to regulate TBX3 expression in occurrence of melanoma, lung, thyroid, breast and other types of cancers12,15,16,20,21,53,54”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
The Introduction reports BRAF/MAPK-induced TBX3 up-regulation in melanoma, and the Results show BRAF/MAPK regulation of TBX3 in thyroid cancer. The Discussion also describes c-Jun activating TBX3 transcription in breast cancer. Our copy does not establish regulation of TBX3 expression in lung cancer or substantiate the claim across other cancer types. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTBX3 is often up-regulated in tumorigenesis and promotes tumor cell proliferation and metastasis, especially during BRAF/MAPK induced tumorigenesis.
“Recently, the oncogenic function of TBX3 draws attention, where TBX3 is often up-regulated in tumorigenesis and promotes tumor cell proliferation and metastasis, especially during BRAF/MAPK induced tumorigenesis12–16.”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
Critical morphogenic and oncogenic signaling pathways, including BMPs, Shh, TGF-β, FGFs, Wnt/β-catenin, and BRAF/MAPK, participate in TBX3 expression regulation, mostly at the transcriptional level.
“Thus, critical morphogenic and oncogenic signaling pathways, such as BMPs17, Shh18, TGF-β19, FGFs20, Wnt/β-catenin21, as well as BRAF/MAPK pathway, participate in TBX3 expression regulation, mostly at the transcriptional level12,15.”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
Infiltration of Gr-1 positive MDSCs is significantly reduced in mPTC/Usp15-/- tumor tissues.
“Also in line with the earlier findings that Tbx3 promotes MDSCs recruitment and immune-suppressive tumor microenvironment (TME) construction15, infiltration of Gr-1 positive MDSCs were significantly reduced in mPTC/Usp15-/- tumor tissues (Fig. 3j).”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
TBX3 has critical oncogenic function in various kinds of tumors.
“We and other groups have converged on the critical oncogenic function of TBX3 in various kinds of tumors9,14,15.”
From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [15]
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Self-citation
- Authors
- Zhang, P., Guan, H., Yuan, S., Cheng, H., Zheng, J., Zhang, Z., Liu, Y., Yu, Y., Meng, Z., Zheng, X., & Zhao, L.
- Affiliations
- Tianjin Medical University General Hospital (CN)
- Guangdong Academy of Medical Sciences (CN)
- Tianjin Medical University (CN)
- Tianjin Medical University Cancer Institute and Hospital (CN)
- Corresponding author
- Zhao, Li
- ORCID
- Venue
- Nature Communications
- Published
- 2022-03-24
- Volume
- 13
- Issue
- 1
- Pages
- 1588-1588
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC8948260
- OpenAlex
- W4220834124
- Cited by
- 86
- References
- 60
- Citations by year
- 2026: 13 · 2025: 26 · 2024: 21 · 2023: 24 · 2022: 2
- FWCI
- 13.53
- Type
- journal article
- Language
- en
- Update notices
- correction (2022-11-17)
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (82073052, 81872235, 81702710, 81971650, 81872169)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- myeloid-derived suppressor cells, papillary thyroid carcinoma, BRAF V600E mutation, MAPK inhibitors, tumor immunosuppression, TBX3, tumor microenvironment, MDSC recruitment, patient stratification, immunotherapy resistance
- MeSH terms
- Myeloid-Derived Suppressor Cells, Thyroid Cancer, Papillary, Humans, Ligands, Mutation, Neoplasm Recurrence, Local, Thyroid Neoplasms, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf, Tumor Microenvironment
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