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Last update 08 May 2025

CXXC5

Last update 08 May 2025

Basic Info

Synonyms

CF5, CXXC finger protein 5, CXXC-type zinc finger protein 5

+ [7]

Introduction

May indirectly participate in activation of the NF-kappa-B and MAPK pathways. Acts as a mediator of BMP4-mediated modulation of canonical Wnt signaling activity in neural stem cells (By similarity). Required for DNA damage-induced ATM phosphorylation, p53 activation and cell cycle arrest. Involved in myelopoiesis. Transcription factor. Binds to the oxygen responsive element of COX4I2 and represses its transcription under hypoxia conditions (4% oxygen), as well as normoxia conditions (20% oxygen) (PubMed:23303788). May repress COX4I2 transactivation induced by CHCHD2 and RBPJ (PubMed:23303788). Binds preferentially to DNA containing cytidine-phosphate-guanosine (CpG) dinucleotides over CpH (H=A, T, and C), hemimethylated-CpG and hemimethylated-hydroxymethyl-CpG (PubMed:29276034).

Drugs associated with CXXC5

KY19334

Target

CXXC5

Mechanism

CXXC5 modulators

Active Org.

CK Regeon Inc.

Originator Org.

CK Regeon Inc.

Active Indication

Nonalcoholic Steatohepatitis [+3]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Wound healing(CK Regeon)

Target

CXXC5

Mechanism

CXXC5 inhibitors

Active Org.

CK Regeon Inc.

Originator Org.

CK Regeon Inc.

Active Indication

Wounds and Injuries

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CXXC5

100 Translational Medicine associated with CXXC5

0 Patents (Medical) associated with CXXC5

169

Literatures (Medical) associated with CXXC5

01 Mar 2025·Bioorganic Chemistry

Targeting Wnt signaling pathway with small-molecule therapeutics for treating osteoporosis

Review

Author: Hussain, Mohd Kamil ; Ahamad, Shakir ; Saquib, Mohammad ; Bhat, Shahnawaz Ali

Small molecules are emerging as potential candidates for treating osteoporosis by activating canonical Wnt signaling. These candidates work either by inhibiting DKK-1, sclerostin, SFRP-1, NOTUM, and S1P lyase or by preventing β-catenin degradation through inhibition of GSK-3β, or by targeting Dvl-CXXC5 and axin/β-catenin interactions. While many of these anti-osteoporotic small molecules are in preclinical development, the paucity of FDA-approved small molecules, or promising candidates, that have progressed to clinical trials for treating bone disorders through this mechanism poses a challenge. Despite advancements in computer-aided drug design, it is rarely employed for designing Wnt signaling activators to treat osteoporosis, and high-throughput screen (HTS) remains the primary method for discovering initial hits. Acknowledging the promising therapeutic potential of these compounds in addressing bone diseases, this review underscores the need for further mechanistic elucidation to enhance our understanding of their applications. Additionally, caution must be exercised in the design of small molecule-based Wnt activators due to their association with oncological risks.

01 Mar 2025·Gene

Novel oncogenes and tumor suppressor genes in Hepatocellular Carcinoma: Carcinogenesis, progression, and therapeutic targets

Review

Author: Shamsinejad, Fatemeh Sadat ; Shahbazi, Taha ; Bolideei, Mansoor ; Rahimi-Farsi, Nasim ; Boustani, Farnaz ; Zangooie, Alireza ; Shoorei, Hamed ; Bostanian, Fatemeh ; Mohseni, Parvin

Hepatocellular carcinoma (HCC) is the primary malignancy affecting the liver and the leading cause of mortality among individuals with cirrhosis. This complex disease is associated with various risk factors, including environmental, pathological, and genetic influences, which dysregulate gene expression crucial for the cell cycle and cellular/molecular pathways. The disruption of the balance between tumor suppressors and proto-oncogenes amplifies the pathogenic cascade. Given its predilection for diseased or cirrhotic livers and late-stage diagnosis, HCC prognosis is typically poor. Current therapies offer limited benefits, with conventional non-specific cytotoxic agents exhibiting suboptimal efficacy. However, molecularly targeted therapies have emerged as a promising avenue, leveraging the strategic inhibition of carcinogenic molecules to provide heightened specificity and potency compared to cytotoxic chemotherapy. Several clinical trials have demonstrated promising outcomes in advanced HCC with targeted pharmacotherapies. Many genes have been implicated in HCC pathogenesis, underscoring the need to elucidate their molecular functions and roles. This has profound implications for early HCC prognostication via biomarkers and for identifying therapeutic targets to impede neoplastic progression. Notably, evidence highlights the pivotal roles of oncogenes and tumor suppressors in HCC pathophysiology. This discourse examines the potential involvement of ABL1, Annexins, FAK, FOX, and KIF as candidate oncogenes, contrasted with SORBS2, HPCAL1, PCDH10, PLAC8, and CXXC5 as plausible tumor suppressors. Their signaling cascades and relevance to HCC prognosis and progression are delineated to identify targets for improving HCC diagnosis, prognostication, and therapy.

01 Dec 2024·Biochemical Pharmacology

Therapeutic targeting of Wnt antagonists by small molecules for treatment of osteoporosis

Review

Author: Chand, Diwan ; Mohanan, Kishor ; Chattopadhyay, Naibedya ; Ahamad, Shakir ; Srivastava, Kinshuk R ; Abhishek Shah, Aarti ; Chourasia, Manish K ; Srivastava, Kinshuk R. ; Porwal, Konica ; Chourasia, Manish K.

Wnt signaling is one of the key regulators of bone development and homeostasis. Wnt signaling regulates key biological events, including stem cell fate and osteoblast and osteoclast activity, leading to the maintenance of bone mass and strength. Wnt ligands are secreted glycoproteins that bind to Frizzled (FZD) receptors and their coreceptors, lipoprotein receptor-related proteins-5/6 (LRP5/6). Binding of Wnts to FZD triggers canonical (β-catenin-dependent) and noncanonical (β-catenin-independent) pathways. In canonical Wnt signaling, stabilized β-catenin translocates to the nucleus, where it promotes osteoblast differentiation by activating target genes, including Runx2 and Osterix. The negative regulators of Wnt or so-called Wnt antagonists, including CXXC5, sFRP, sclerostin, DKK1, and Notum, compete for Fzd binding, attenuating Wnt signaling. The critical roles of Wnt signaling in bone homeostasis have been established by various bone diseases caused by mutations in Wnt signaling pathways. Loss-of-function mutations in the LRP5 gene cause osteoporosis-pseudoglioma syndrome, whereas gain-of-function mutations are linked to osteopetrosis characterized by high bone density. Sclerosteosis and Van Buchem disease are caused by mutations affecting the SOST gene, which encodes sclerostin, a natural inhibitor of Wnt signalling. Loss-of-function mutations in SOST result in excessive bone growth, markedly increased bone density, and other skeletal abnormalities due to uncontrolled Wnt activity. Considering the clinical relevance of Wnt signaling, targeting Wnt inhibitors is being intensely pursued using small molecules that act by inhibiting endogenous Wnt agonists. We used a computational biology approach to review current data on pharmacophores of Wnt antagonists, assessing their potential as therapeutic candidates for postmenopausal osteoporosis.

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CXXC5

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