Tight junction protein CLDN17 serves as a tumor suppressor to reduce the invasion and migration of oral cancer cells by inhibiting epithelial-mesenchymal transition

Xu, Yani; Deng, Mingsi; Liu, Yunfeng; Yao, Jun; Xiao, Zi‐Yi

doi:10.1016/j.archoralbio.2021.105301

Cited by 15 publications

(7 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another in vitro study investigated the role of CLDN17 in head and neck cancer cells, where CLDN17 gene expression profiles in oral cancer tissues were analyzed. There was an association of lower CLDN17 expression with higher tumor staging, poorer tumor histological grading, and worse clinical prognosis [119]. Therefore, CLDN17 was proposed to have a tumor suppressor effect in oral cancer by inhibiting epithelial-mesenchymal transformation, tumor invasion, and migration.…”

Section: Role Of Claudins In Cancermentioning

confidence: 99%

Claudins in Cancer: A Current and Future Therapeutic Target

Hana,

Thaw Dar,

Galo Venegas

et al. 2024

IJMS

View full text Add to dashboard Cite

Claudins are a family of 27 proteins that have an important role in the formation of tight junctions. They also have an important function in ion exchange, cell mobility, and the epithelial-to-mesenchymal transition, the latter being very important in cancer invasion and metastasis. Therapeutic targeting of claudins has been investigated to improve cancer outcomes. Recent evidence shows improved outcomes when combining monoclonal antibodies against claudin 18.2 with chemotherapy for patients with gastroesophageal junction cancer. Currently, chimeric antigen receptor T-cells targeting claudin 18 are under investigation. In this review, we will discuss the major functions of claudins, their distribution in the normal as well as cancerous tissues, and their effect in cancer metastasis, with a special focus on the therapeutic targeting of claudins to improve cancer outcomes.

show abstract

Section: Role Of Claudins In Cancermentioning

confidence: 99%

Claudins in Cancer: A Current and Future Therapeutic Target

Hana,

Thaw Dar,

Galo Venegas

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

“…As of today, the precise role of CLDN17 in physiology and pathology is unknown, except for some cancer cells in vitro [ 25 , 26 , 27 ]. Literature on CLDN17 is scarce, and the reagents and tools to study the role of CLDN17 in cell–cell and blood–tissue-barrier regulation are limited.…”

Section: Introductionmentioning

confidence: 99%

Claudin-17 Deficiency in Mice Results in Kidney Injury Due to Electrolyte Imbalance and Oxidative Stress

Adil

Parvathagiri²,

Verma³

et al. 2022

Cells

View full text Add to dashboard Cite

The multi-gene claudin (CLDN) family of tight junction proteins have isoform-specific roles in blood–tissue barrier regulation. CLDN17, a putative anion pore-forming CLDN based on its structural characterization, is assumed to regulate anion balance across the blood-tissue barriers. However, our knowledge about CLDN17 in physiology and pathology is limited. The current study investigated how Cldn17 deficiency in mice affects blood electrolytes and kidney structure. Cldn17–/– mice revealed no breeding abnormalities, but the newborn pups exhibited delayed growth. Adult Cldn17–/– mice displayed electrolyte imbalance, oxidative stress, and injury to the kidneys. Ingenuity pathway analysis followed by RNA-sequencing revealed hyperactivation of signaling pathways and downregulation of SOD1 expression in kidneys associated with inflammation and reactive oxygen species generation, demonstrating the importance of Cldn17 in the maintenance of electrolytes and reactive oxygen species across the blood-tissue barrier.

show abstract

“…The claudin family of membrane proteins plays a central role in the structure and function of tight junctions ( 4 ). In humans, claudin-1, 3–5, 7, 8, 10, 12, 18, and 23 are most abundantly expressed ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

Claudin-18 expression under hyperoxia in neonatal lungs of bronchopulmonary dysplasia model rats

et al. 2022

View full text Add to dashboard Cite

BackgroundBronchopulmonary dysplasia (BPD) is characterized by impaired alveolar and microvascular development. Claudin-18 is the only known lung-specific tight junction protein affecting the development and transdifferentiation of alveolar epithelium.ObjectiveWe aimed to explore the changes in the expression of claudin-18, podoplanin, SFTPC, and the canonical WNT pathway, in a rat model of hyperoxia-induced BPD, and to verify the regulatory relationship between claudin-18 and the canonical WNT pathway by cell experiments.MethodsA neonatal rat and cell model of BPD was established by exposing to hyperoxia (85%). Hematoxylin and eosin (HE) staining was used to confirm the establishment of the BPD model. The mRNA levels were assessed using quantitative real-time polymerase chain reaction(qRT-PCR). Protein expression levels were determined using western blotting, immunohistochemical staining, and immunofluorescence.ResultsAs confirmed by HE staining, the neonatal rat model of BPD was successfully established. Compared to that in the control group, claudin-18 and claudin-4 expression decreased in the hyperoxia group. Expression of β-catenin in the WNT signaling pathway decreased, whereas that of p-GSK-3β increased. Expression of the AEC II marker SFTPC initially decreased and then increased, whereas that of the AEC I marker podoplanin increased on day 14 (P < 0.05). Similarly, claudin-18, claudin-4, SFTPC and β-catenin were decreased but podoplanin was increased when AEC line RLE-6TN exposed to 85% hyperoxia. And the expression of SFTPC was increased, the podoplanin was decreased, and the WNT pathway was upregulated when claudin-18 was overexpressed.ConclusionsClaudin-18 downregulation during hyperoxia might affect lung development and maturation, thereby resulting in hyperoxia-induced BPD. Additionally, claudin-18 is associated with the canonical WNT pathway and AECs transdifferentiation.

show abstract

Tight junction protein CLDN17 serves as a tumor suppressor to reduce the invasion and migration of oral cancer cells by inhibiting epithelial-mesenchymal transition

Cited by 15 publications

References 39 publications

Claudins in Cancer: A Current and Future Therapeutic Target

Claudins in Cancer: A Current and Future Therapeutic Target

Claudin-17 Deficiency in Mice Results in Kidney Injury Due to Electrolyte Imbalance and Oxidative Stress

Claudin-18 expression under hyperoxia in neonatal lungs of bronchopulmonary dysplasia model rats

Contact Info

Product

Resources

About