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Last update 08 May 2025

POU3F3

Last update 08 May 2025

Basic Info

Synonyms

Brain-1, Brain-specific homeobox/POU domain protein 1, Brn-1

+ [9]

Introduction

Transcription factor that acts synergistically with SOX11 and SOX4. Plays a role in neuronal development (PubMed:31303265). Is implicated in an enhancer activity at the embryonic met-mesencephalic junction; the enhancer element contains the octamer motif (5'-ATTTGCAT-3') (By similarity).

Drugs associated with POU3F3

WO2022203429

Patent Mining

Target

POU3F3

Mechanism-

Active Org.

Chong Kun Dang Pharmaceutical Corp.

Originator Org.

Chong Kun Dang Pharmaceutical Corp.

Active Indication

Nervous System Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with POU3F3

100 Translational Medicine associated with POU3F3

0 Patents (Medical) associated with POU3F3

157

Literatures (Medical) associated with POU3F3

01 Apr 2025·Advanced Science

Phosphorylation of POU3F3 Mediated Nuclear Translocation Promotes Proliferation in Non‐Small Cell Lung Cancer through Accelerating ATP5PF Transcription and ATP Production

Article

Author: Yao, Hao‐Tao ; Zhou, Dan‐Yang ; Gu, Jia‐Xin ; Liu, Chao‐Ling ; An, Zhao‐Rong ; Zheng, Bin ; Li, Xia‐Qing ; Zeng, Qi‐Gang ; Sun, Yong ; Xue, Ling‐Na ; Huang, Ruo‐Tong ; Li, Le ; Fan, Jun ; Dai, Yong ; Chang, Tao

AbstractTargeting oxidative phosphorylation (OXPHOS) through inhibiting the electron transport chain (ETC) has shown promising pre‐clinical efficacy in cancer therapy. Although aerobic glycolysis is a hallmark of cancer, emerging evidence suggest OXPHOS is frequently enhanced, providing metabolic advantages for cell proliferation, metastasis, and drug resistance in a variety of aggressive cancer types including non‐small cell lung cancer (NSCLC), yet the underlying molecular mechanisms remain elusive. Here it is reported that POU‐domain containing family protein POU3F3 is translocated into the nuclei of NSCLC cell lines harboring mutant RAS, where it activates transcription of ATP5PF, an essential component of mitochondrial ATP synthase and consequent ATP production, leading to enhanced NSCLC proliferation and migration. Moreover, it is further found out that ERK1 phosphorylates POU3F3 at the S393 site in the cytoplasm and promotes the nuclear translocation of POU3F3 via receptor importin β1 in RAS mutant NSCLC cells. Mechanistically, RNA sequencing analysis combined with chromatin immunoprecipitation (ChIP) assay revealed that POU3F3 binds to the promoter of ATP5PF, leading to enhanced ATP5PF transcription and ATP production. Together, this study uncovers a novel RAS‐POU3F3‐ATP5PF axis in facilitating NSCLC progression, providing a new perspective on the understanding of molecular mechanisms for NSCLC progression.

15 Jan 2025·Biology Open

A subpopulation of cortical neurons altered by mutations in the autism risk gene DDX3X

Article

Author: Boitnott, Andrea ; De Rubeis, Silvia ; Garcia-Forn, Marta ; von Mueffling, Alexa ; Ola, Praise ; Park, Yeaji ; Flores, Michael A.

ABSTRACTCell fate decisions during cortical development sculpt the identity of long-range connections that subserve complex behaviors. These decisions are largely dictated by mutually exclusive transcription factors, including CTIP2/Bcl11b for subcerebral projection neurons and BRN1/Pou3f3 for intra-telencephalic projection neurons. We have recently reported that the balance of cortical CTIP2-expressing neurons is altered in a mouse model of DDX3X syndrome, a female-biased neurodevelopmental disorder associated with intellectual disability, autism spectrum disorder, and significant motor challenges. Here, we studied the developmental dynamics of a subpopulation of cortical neurons co-expressing CTIP2 and BRN1. We found that CTIP2+BRN1+ neurons are born during early phases of neurogenesis like other CTIP2+ neurons, peak in expression during perinatal life, and persist in adult brains. We also found that CTIP2+BRN1+ neurons are excessive in number in prenatal and mature cortical motor areas of Ddx3x mutant mice, translating into altered laminar distribution of subcerebral projection neurons extending axons to the brainstem. These findings underscore the critical role of molecular specification during cortical development in health and disease.

01 Dec 2024·Critical Reviews in Oncology/Hematology

Targeted therapy with polymeric nanoparticles in PBRM1-mutant biliary tract cancers: Harnessing DNA damage repair mechanisms

Review

Author: Bhattacharya, Sankha ; Wagh, Hrushikesh

Biliary tract cancers (BTCs) are aggressive malignancies with a dismal prognosis that require intensive targeted therapy. Approximately 10 % of BTCs have PBRM1 mutations, which impede DNA damage repair pathways and make cancer cells more susceptible to DNA-damaging chemicals. This review focus on development of poly(lactic-co-glycolic acid) (PLGA)-based nanoparticles targeting delivery system to selectively deliver chemotherapy into PBRM1-deficient BTC cells. These nanoparticles improve therapy efficacy by increasing medication targeting and retention at tumour locations. In preclinical studies, pharmacokinetic profile of this nanoparticle was encouraging and supported its ability to achieve extended circulation time with high drug accumulation in tumor. The review also highlights potential of Pou3F3:I54N to expedite bioassays for patient selection in BTC targeted therapies.

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POU3F3

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