Affinage

PRR11

Proline-rich protein 11 · UniProt Q96HE9

Length
360 aa
Mass
40.1 kDa
Annotated
2026-06-10
37 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRR11 is a cell-cycle-regulated, predominantly cytoplasmic proline-rich protein whose expression peaks from late S phase to mitosis and is required for orderly S-to-G2/M progression, with loss causing S-phase and G2/M arrest and mitotic defects such as multipolar spindles and multinucleation (PMID:23246489, PMID:25666944). Mechanistically, cytoplasmic PRR11 uses its proline-rich region to associate with and recruit the ARP2/3 complex, driving F-actin polymerization and filopodia formation, supporting FAK-Y397 activation and focal adhesion turnover, and maintaining proper nuclear lamina assembly; domain mapping shows the proline-rich region (notably aa 185–200) is essential for these actin-dependent effects (PMID:32169900, PMID:35005120). PRR11 also nucleates growth-factor signaling: its proline-rich motif binds the PI3K regulatory subunit p85α to suppress p85α homodimerization and enhance IRS1-associated p110–p85α PI3K activity, and it interacts with GRB2, together activating PI3K-AKT signaling (PMID:33127913, PMID:41309933). In the nucleus, PRR11 interacts with E2F1 to modulate its stability and transcriptional output, including activation of PTTG1 (PMID:34499617, PMID:36060253). PRR11 additionally stabilizes DHODH by blocking HERC4-mediated K306 polyubiquitination, conferring ferroptosis resistance (PMID:38838551), and its own protein level is controlled by the deubiquitinase OTUB1 (PMID:41575699). PRR11 is transcribed from a bidirectional promoter shared head-to-head with SKA2 that is directly bound and transactivated by NF-Y and repressed by wild-type p53 through displacement of NF-Y (PMID:26162986, PMID:28257042).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2012 Medium

    Established that PRR11 is a cell-cycle-dependent gene functionally required for cell proliferation, defining it as a candidate cell-cycle regulator rather than a passively co-expressed transcript.

    Evidence RNAi knockdown with flow cytometry, colony formation, and xenograft in HeLa and lung cancer cells

    PMID:23246489

    Open questions at the time
    • No molecular mechanism for the S-phase arrest identified
    • Subcellular localization and partners unknown at this stage
  2. 2015 Medium

    Defined where and when PRR11 acts by showing it is largely cytoplasmic, accumulating from late S phase to telophase, and that its loss produces late-S/G2/M arrest and mitotic catastrophe.

    Evidence Immunofluorescence, cell synchronization, siRNA knockdown, flow cytometry in cell lines

    PMID:25666944

    Open questions at the time
    • No direct molecular effectors of the mitotic phenotype identified
    • Mechanism of premature chromatin condensation unexplained
  3. 2015 High

    Resolved how PRR11 transcription is wired by mapping an 80-bp bidirectional promoter shared with SKA2 that NF-Y directly binds and transactivates, explaining co-regulation of the two genes.

    Evidence 5'-RACE, serial luciferase reporters, EMSA, ChIP, NF-Y depletion

    PMID:26162986

    Open questions at the time
    • Upstream signals controlling NF-Y at this promoter not yet defined
    • Functional relationship between PRR11 and SKA2 proteins not addressed
  4. 2017 High

    Connected PRR11 to tumor-suppressor control by showing wild-type p53 represses the bidirectional promoter indirectly through association with NF-Y and reduction of NF-Y occupancy.

    Evidence Luciferase reporters, mutagenesis, co-IP, ChIP, siRNA depletion in lung cancer cells

    PMID:28257042

    Open questions at the time
    • Whether p53 acts at this promoter in non-lung tissues not tested
    • Does not establish PRR11 protein-level consequences of p53 activation
  5. 2017 Low

    Linked PRR11 to Akt/mTOR and autophagy, indicating a signaling role beyond transcriptional regulation.

    Evidence siRNA knockdown with immunoblotting of LC3-II, p62, p-Akt, p-mTOR in NSCLC cells

    PMID:30258945

    Open questions at the time
    • No pathway rescue or reconstitution; correlation only
    • Direct molecular link between PRR11 and Akt/mTOR not shown here
  6. 2018 Medium

    Identified upstream non-coding regulators by validating PRR11 mRNA as a direct miR-195 target and as a functional effector downstream of the DLX6-AS1/miR-144 ceRNA axis.

    Evidence Dual-luciferase assays, microarray, rescue proliferation assays, xenografts

    PMID:29393495 PMID:30551440

    Open questions at the time
    • ceRNA model (DLX6-AS1/miR-144) is indirect and single-lab
    • Physiological relevance of these miRNA interactions in normal tissue untested
  7. 2019 Medium

    Extended the p53–NF-Y repression of PRR11 to breast cancer and showed endogenous p53 induction lowers PRR11, while defining downstream dysregulated targets (CDK6, TPM3, USP12).

    Evidence Reporter assays, adriamycin-induced p53 activation, siRNA, western blot, qRT-PCR

    PMID:30760381

    Open questions at the time
    • Downstream gene changes are correlative, not mechanistically dissected
    • Direct vs indirect control of each target unresolved
  8. 2020 High

    Provided the first direct molecular function for cytoplasmic PRR11 by showing it recruits the ARP2/3 complex to drive F-actin polymerization and proper nuclear lamina assembly, with domain mapping localizing the activity.

    Evidence Actin polymerization assay, immunofluorescence, truncation/deletion mutants, ARP2/3 inhibitor rescue in NSCLC cells

    PMID:32169900

    Open questions at the time
    • Whether PRR11 directly nucleates or acts as an ARP2/3 adaptor not fully resolved
    • Link between actin defects and the cell-cycle phenotype not mechanistically closed
  9. 2020 High

    Defined a growth-factor signaling mechanism: PRR11's proline-rich motif binds p85α to block its homodimerization, enhancing IRS1-associated PI3K activity and driving endocrine resistance.

    Evidence Co-IP, p85α homodimerization assay, IRS1 binding assay, PI3K inhibitor sensitivity in ER+ breast cancer

    PMID:33127913

    Open questions at the time
    • Structural basis of the PRR11–p85α interaction not determined
    • Relative contribution of PI3K vs actin functions to proliferation unresolved
  10. 2020 Low

    Associated PRR11 protein stability with deubiquitinase USP34, hinting at post-translational regulation.

    Evidence shRNA knockdown of USP34, western blot of PRR11 and p-p38, xenograft

    PMID:32110045

    Open questions at the time
    • Direct deubiquitination of PRR11 by USP34 not demonstrated
    • Western blot association only, no reciprocal validation
  11. 2021 Medium

    Refined the cytoskeletal role to filopodia (not lamellipodia) formation via Arp2 co-localization and showed PRR11 controls integrin β1 activation, FAK phosphorylation, and focal adhesion turnover.

    Evidence siRNA, co-localization, deletion mutants, flow cytometry for active integrin β1, pFAK western blot in NSCLC cells

    PMID:35005120

    Open questions at the time
    • Mechanism linking PRR11 to integrin β1 activation state unknown
    • Single lab; in vivo motility role not tested
  12. 2021 Medium

    Revealed a nuclear, transcription-modulating arm in which PRR11 interacts with E2F1 to affect its stability and, on the PTTG1 promoter, increase PTTG1 transcription, with c-Myc identified as an upstream activator of PRR11.

    Evidence Co-IP, protein stability assays, ChIP, RNA-seq, nuclear fractionation in ccRCC and other cancer cells

    PMID:34499617 PMID:36060253

    Open questions at the time
    • Opposing reports of E2F1 destabilization vs cooperative promoter activity not reconciled
    • How a proline-rich protein modulates E2F1 stability mechanistically unclear
  13. 2021 Low

    Placed PRR11 expression downstream of additional oncogenic transcriptional inputs (GLI1/2 Hedgehog signaling) and non-coding cascades (lncRNA CCDC26/CELF2/circRNA_ANKIB1).

    Evidence GLI1/2 inhibitor and siRNA with RNA-seq; RNA pull-down and RNA-IP in leukemia cells

    PMID:33439746 PMID:33477943

    Open questions at the time
    • GLI direct binding to the PRR11 promoter not shown (epistasis only)
    • ncRNA regulation of PRR11 is indirect and single-lab
  14. 2023 Low

    Showed the ELF1→PRR11→ARP2/3 axis operates outside cancer, supporting trophoblast proliferation and motility.

    Evidence ChIP for ELF1, western blot, immunofluorescence, MTT and Transwell in trophoblast cells

    PMID:37641376

    Open questions at the time
    • Mechanistic follow-up limited; single study
    • Physiological role in placentation not established
  15. 2024 High

    Uncovered a metabolic/redox function: PRR11 binds DHODH and blocks HERC4-mediated K306 polyubiquitination, stabilizing DHODH and conferring ferroptosis resistance.

    Evidence Co-IP, ubiquitination assays with K306 mutagenesis, HERC4 recruitment assay, in vivo glioblastoma models

    PMID:38838551

    Open questions at the time
    • Whether this ferroptosis role generalizes beyond glioblastoma untested
    • How cytoplasmic PRR11 balances actin, PI3K, and DHODH functions unresolved
  16. 2025 Medium

    Added GRB2 as a direct PRR11 partner driving PI3K-AKT activation and showed CRISPRi repression of the entire PRR11-SKA2-miR301a/454 unit suppresses growth, cycle, and motility.

    Evidence Co-IP for PRR11–GRB2, CRISPRi, functional assays, mouse tumor models in lung cancer

    PMID:41309933

    Open questions at the time
    • Relative contribution of GRB2 vs p85α to PI3K activation not dissected
    • Individual gene contributions within the repressed unit not separated
  17. 2026 Medium

    Identified OTUB1 as a deubiquitinase that stabilizes PRR11 and linked PRR11 to Wnt/β-catenin activation via DKK3 suppression in retinoblastoma.

    Evidence Co-IP/mass spectrometry, proteomic analysis, knockdown, in vitro and in vivo tumor assays

    PMID:41575699

    Open questions at the time
    • Direct deubiquitination of PRR11 by OTUB1 vs indirect stabilization not fully separated
    • Mechanism by which PRR11 suppresses DKK3 unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how PRR11's multiple molecular activities — cytoskeletal ARP2/3 recruitment, PI3K-AKT signaling, E2F1/transcriptional modulation, and DHODH stabilization — are integrated within a single cell-cycle program, and whether these are coupled or context-specific functions.
  • No structural model of PRR11 or its proline-rich interaction surfaces
  • No unifying assay testing which activity is rate-limiting for the cell-cycle phenotype
  • Native protein complexes containing PRR11 not characterized stoichiometrically

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0008092 cytoskeletal protein binding 2 GO:0098772 molecular function regulator activity 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 2 R-HSA-1640170 Cell Cycle 2 R-HSA-74160 Gene expression (Transcription) 2
Partners
ARP2/3DHODHE2F1GRB2HERC4OTUB1PIK3R1SKA2

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 PRR11 is periodically expressed in a cell cycle-dependent manner; RNAi-mediated silencing causes significant S phase arrest and growth retardation in HeLa and lung cancer cells, establishing a role in cell cycle progression. RNAi knockdown, flow cytometry, colony formation, xenograft The international journal of biochemistry & cell biology Medium 23246489
2015 PRR11 and SKA2 are oriented head-to-head with an intergenic spacer <500 bp; a minimal 80-bp region functions as a core bidirectional promoter, and NF-Y directly binds and transactivates this promoter to drive expression of both genes. 5'-RACE, serial luciferase reporter assays, EMSA, ChIP, siRNA-mediated NF-Y depletion Biochimica et biophysica acta High 26162986
2015 PRR11 is expressed largely in the cytoplasm; its expression starts to increase in late S phase and is retained until just before mitotic telophase. siRNA knockdown causes arrest in the late S phase and G2/M, leading to mitotic defects (multipolar spindles, multiple nuclei). Forced PRR11 expression induces premature chromatin condensation (PCC) and apoptosis. Immunofluorescence, siRNA knockdown, cell synchronization, flow cytometry, dNTP supplementation Biochemical and biophysical research communications Medium 25666944
2017 p53 negatively regulates PRR11-SKA2 bidirectional transcription indirectly through NF-Y: wild-type p53 (but not mutant p53) represses the promoter in an NF-Y binding site-dependent manner; co-IP shows p53 associates with NF-Y in lung cancer cells; ChIP shows p53 reduces NF-Y occupancy at the PRR11-SKA2 promoter; NF-YB depletion attenuates p53-mediated repression. Luciferase reporter assay, deletion/mutation analysis, co-immunoprecipitation, ChIP, siRNA depletion International journal of molecular sciences High 28257042
2017 PRR11 silencing in NSCLC cells inactivates the Akt/mTOR signaling pathway, enhances autophagosome formation, and upregulates LC3-II while downregulating p62, demonstrating a role in autophagy regulation. siRNA knockdown, immunoblotting (LC3-II, p62, p-Akt, p-mTOR), CCK-8, clone formation assay Genes & diseases Low 30258945
2019 p53 (wild-type) represses the PRR11-SKA2 bidirectional promoter in breast cancer cells; adriamycin-induced p53 activation reduces PRR11 and SKA2 expression; NF-Y is essential for PRR11 but not SKA2 expression in this context; PRR11/SKA2 knockdown dysregulates downstream genes CDK6, TPM3, and USP12. Luciferase reporter assay, drug-induced p53 activation, siRNA, western blot, qRT-PCR BMB reports Medium 30760381
2020 Cytoplasmic PRR11 associates with and recruits the ARP2/3 complex, facilitating F-actin polymerization and organization in NSCLC cells; dysregulation leads to abnormal nuclear lamina assembly and chromatin reorganization. Truncation mapping showed deletion of either N or C terminus abrogates F-actin effects; deletion of aa 100–184 or 100–200 induces actin comet tails. ARP2/3 inhibition abolishes PRR11 overexpression-induced F-actin changes. Immunofluorescence, actin polymerization assay, siRNA knockdown, truncation/deletion mutants, ARP2/3 inhibitor The Journal of biological chemistry High 32169900
2020 The proline-rich motif of PRR11 interacts with the p85α regulatory subunit of PI3K, suppressing p85α homodimerization and thereby enhancing insulin-stimulated binding of p110-p85α heterodimers to IRS1 and activation of PI3K, driving estrogen-independent proliferation and endocrine resistance in ER+ breast cancer. Co-IP, functional proliferation assays, PI3K inhibitor sensitivity assays, genetic knockdown/overexpression Nature communications High 33127913
2021 PRR11 recruits and co-localizes with Arp2 at membrane protrusions to promote filopodia formation (but not lamellipodia); deletion of the proline-rich region 2 (aa 185–200) abrogates filopodia formation. PRR11 depletion increases active integrin β1 on the cell surface and reduces FAK-Y397 phosphorylation, repressing focal adhesion turnover and cell motility in NSCLC cells. siRNA knockdown, immunofluorescence/co-localization, PRR11 deletion mutants, flow cytometry (active integrin β1), western blot (pFAK) Genes & diseases Medium 35005120
2021 PRR11 interacts with E2F1 protein and promotes degradation/reduces the stability of E2F1 in ccRCC cells, thereby affecting cell cycle progression; c-Myc transcription factor binds the PRR11 promoter and promotes PRR11 expression in ccRCC. Co-immunoprecipitation, protein stability assay, ChIP (c-Myc at PRR11 promoter), siRNA knockdown JCI insight Medium 34499617
2021 PRR11 interacts with E2F1 on the PTTG1 promoter region (as shown by co-IP and promoter assays) to increase PTTG1 transcription, and PRR11 can be detected in the nucleus; this PRR11-E2F1-PTTG1 axis promotes cell cycle progression and cancer cell proliferation. Co-immunoprecipitation, RNA-seq, ChIP/promoter analysis, siRNA knockdown, nuclear fractionation Frontiers in molecular biosciences Medium 36060253
2021 Hedgehog pathway inhibition (GLI1/2 inhibitor GANT-61 or GLI1/2-siRNA) decreases PRR11 and SKA2 expression in lung squamous cell carcinoma cells, placing PRR11 expression downstream of GLI1/2 in the Hedgehog pathway. siRNA knockdown of GLI1/2, pharmacological inhibitor (GANT-61), RNA sequencing, RT-PCR Genes Low 33477943
2021 lncRNA CCDC26 interacts with CELF2 RNA-binding protein (confirmed by RNA pull-down and RNA-IP) and upregulates PRR11 protein by sponging miR-195a-5p via circRNA_ANKIB1; elevated PRR11 activates PI3K/AKT and NF-κB pathways in myeloid leukemia cells. RNA pull-down, RNA-IP, luciferase reporter, miRNA inhibitor, western blot Cell transplantation Low 33439746
2023 ELF1 transcription factor binds the PRR11 promoter and promotes its transcriptional activation; PRR11 in turn recruits the ARP2/3 complex to promote F-actin polymerization and FAK activation in trophoblast cells, supporting proliferation and motility. ChIP (ELF1 at PRR11 promoter), western blot, immunofluorescence, MTT, Transwell assay American journal of reproductive immunology Low 37641376
2024 PRR11 directly binds to and stabilizes DHODH protein; PRR11 inhibits binding of E3 ubiquitin ligase HERC4 to DHODH, suppressing HERC4-mediated polyubiquitination of DHODH at K306, thereby preventing its proteasomal degradation and conferring ferroptosis resistance in glioblastoma cells. Co-IP, ubiquitination assay, site-directed mutagenesis (K306), PRR11 depletion, in vitro and in vivo functional assays Redox biology High 38838551
2025 PRR11 interacts with GRB2 (while SKA2 interacts with EGFR) to robustly activate the PI3K-AKT pathway in lung cancer cells; CRISPRi-mediated repression of the entire PRR11-SKA2-miR301a/454 transcription unit inhibits cell growth, cell cycle progression, and cell motility. Co-immunoprecipitation (PRR11–GRB2 interaction), CRISPRi, functional cell assays, mouse tumor models Oncogene Medium 41309933
2026 OTUB1 deubiquitinase interacts with PRR11 and stabilizes it in retinoblastoma cells (identified by co-IP/mass spectrometry); PRR11 suppresses DKK3 expression, leading to aberrant Wnt/β-catenin pathway activation, cyclin D1 upregulation, and S/G2M cell cycle progression. Co-IP/mass spectrometry, proteomic analysis, functional knockdown, in vitro and in vivo tumor assays Science China. Life sciences Medium 41575699
2018 miR-195 directly targets PRR11 mRNA (validated by dual-luciferase assay); PRR11 overexpression abrogates the suppressive effects of miR-195 on prostate cancer cell proliferation, tube formation, and cell cycling, establishing PRR11 as a functional downstream target of the miR-195 axis. Dual-luciferase assay, RNA microarray, in vitro proliferation/tube formation assays, xenograft model Oncology reports Medium 29393495
2018 lncRNA DLX6-AS1 acts as a competing endogenous RNA (ceRNA) for miR-144, upregulating PRR11 expression; PRR11 overexpression reverses DLX6-AS1-knockdown-mediated suppression of NSCLC cell proliferation and invasion, placing PRR11 downstream of the DLX6-AS1/miR-144 axis. Luciferase reporter assay, siRNA knockdown, western blot, qRT-PCR, xenograft assay Biomedicine & pharmacotherapy Low 30551440
2020 USP34 deubiquitinase knockdown significantly downregulates PRR11 protein levels in pancreatic cancer PANC-1 cells, suggesting USP34 promotes PRR11 protein stability; this is accompanied by inactivation of p38 MAPK signaling. shRNA knockdown of USP34, western blot (PRR11, p-p38), xenograft in vivo model OncoTargets and therapy Low 32110045

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 PRR11 is a novel gene implicated in cell cycle progression and lung cancer. The international journal of biochemistry & cell biology 71 23246489
2015 The gene pair PRR11 and SKA2 shares a NF-Y-regulated bidirectional promoter and contributes to lung cancer development. Biochimica et biophysica acta 54 26162986
2018 Knockdown of lncRNA DLX6-AS1 inhibits cell proliferation, migration and invasion while promotes apoptosis by downregulating PRR11 expression and upregulating miR-144 in non-small cell lung cancer. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 47 30551440
2018 miR-195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression. Oncology reports 43 29393495
2020 Proline rich 11 (PRR11) overexpression amplifies PI3K signaling and promotes antiestrogen resistance in breast cancer. Nature communications 37 33127913
2015 PRR11 regulates late-S to G2/M phase progression and induces premature chromatin condensation (PCC). Biochemical and biophysical research communications 35 25666944
2024 A targetable PRR11-DHODH axis drives ferroptosis- and temozolomide-resistance in glioblastoma. Redox biology 31 38838551
2017 Silencing of PRR11 suppresses cell proliferation and induces autophagy in NSCLC cells. Genes & diseases 26 30258945
2017 The PRR11-SKA2 Bidirectional Transcription Unit Is Negatively Regulated by p53 through NF-Y in Lung Cancer Cells. International journal of molecular sciences 24 28257042
2019 PRR11 and SKA2 gene pair is overexpressed and regulated by p53 in breast cancer. BMB reports 23 30760381
2018 PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 22 30165366
2017 Expression of PRR11 protein and its correlation with pancreatic cancer and effect on survival. Oncology letters 18 28599413
2020 Proline-rich 11 (PRR11) drives F-actin assembly by recruiting the actin-related protein 2/3 complex in human non-small cell lung carcinoma. The Journal of biological chemistry 17 32169900
2020 Downregulation of USP34 Inhibits the Growth and Migration of Pancreatic Cancer Cells via Inhibiting the PRR11. OncoTargets and therapy 16 32110045
2021 LncRNA CCDC26 Interacts with CELF2 Protein to Enhance Myeloid Leukemia Cell Proliferation and Invasion via the circRNA_ANKIB1/miR-195-5p/PRR11 Axis. Cell transplantation 15 33439746
2019 MicroRNA-211-5p promotes apoptosis and inhibits the migration of osteosarcoma cells by targeting proline-rich protein PRR11. Biochemistry and cell biology = Biochimie et biologie cellulaire 15 31075210
2021 PRR11 promotes ccRCC tumorigenesis by regulating E2F1 stability. JCI insight 14 34499617
2020 PRR11 and SKA2 promote the proliferation, migration and invasion of esophageal carcinoma cells. Oncology letters 14 32565988
2021 Down-regulation of PRR11 affects the proliferation, migration and invasion of osteosarcoma by inhibiting the Wnt/β-catenin pathway. Journal of Cancer 11 34659555
2021 PRR11 induces filopodia formation and promotes cell motility via recruiting ARP2/3 complex in non-small cell lung cancer cells. Genes & diseases 11 35005120
2019 Overexpression of PRR11 promotes tumorigenic capability and is associated with progression in esophageal squamous cell carcinoma. OncoTargets and therapy 11 31040705
2022 miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11. Computational and mathematical methods in medicine 10 35126622
2019 The oncogenic potential of PRR11 gene in Tongue Squamous Cell Carcinoma cells. Journal of Cancer 10 31258760
2022 PRR11 Promotes Proliferation and Migration of Colorectal Cancer through Activating the EGFR/ERK/AKT Pathway via Increasing CTHRC1. Annals of clinical and laboratory science 9 35181621
2021 PRR11 unveiled as a top candidate biomarker within the RBM3-regulated transcriptome in pancreatic cancer. The journal of pathology. Clinical research 9 34379360
2021 MicroRNA-26b-5p suppresses the proliferation of tongue squamous cell carcinoma via targeting proline rich 11 (PRR11). Bioengineered 9 34488538
2022 PRR11 promotes cell proliferation by regulating PTTG1 through interacting with E2F1 transcription factor in pan-cancer. Frontiers in molecular biosciences 6 36060253
2022 PRR11 in Malignancies: Biological Activities and Targeted Therapies. Biomolecules 6 36551227
2020 Ultrasonic irradiation and SonoVue microbubbles-mediated RNA interference targeting PRR11 inhibits breast cancer cells proliferation and metastasis, but promotes apoptosis. Bioscience reports 6 33057583
2021 HEDGEHOG/GLI Modulates the PRR11-SKA2 Bidirectional Transcription Unit in Lung Squamous Cell Carcinomas. Genes 5 33477943
2025 PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial-Mesenchymal Transition. Cancer medicine 2 40062654
2023 Proline-rich 11 (PRR11) promotes the progression of cutaneous squamous cell carcinoma by activating the EGFR signaling pathway. Molecular carcinogenesis 2 36727626
2025 Overexpressed PRR11-SKA2-miR301a/454 bidirectional transcription unit essentially and coordinately promotes PI3K-AKT pathway activation and lung cancer progression. Oncogene 1 41309933
2023 [Corrigendum] miR‑195 inhibits cell proliferation and angiogenesis in human prostate cancer by downregulating PRR11 expression. Oncology reports 1 36825583
2023 ELF1/PRR11/ARP2/3 promoted trophoblast cells proliferation and motility in early pregnancy. American journal of reproductive immunology (New York, N.Y. : 1989) 1 37641376
2026 PRR11 as a newly identified oncogenic driver in retinoblastoma. Science China. Life sciences 0 41575699
2023 Retracted: miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11. Computational and mathematical methods in medicine 0 37811303

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