Basal cell carcinoma on the ventral site of the finger with an intronic deletion of <i>SUFU</i> gene

Takata, Mayumi; Komori, Takaya; Ishida, Yoshihiro; Fujimoto, Masakazu; Ogawa, Seishi; Kabashima, Kenji

doi:10.1111/jdv.17694

Cited by 1 publication

(1 citation statement)

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“…Patients with eyelid BCC have many postoperative complications and are prone to develop resistance to existing pharmacological treatments, therefore, new therapeutic targets must be identi ed. Although various pathways have been reported to be activated in eyelid BCC, such as the Hedgehog/GLI, WNT, TGF-β, and JAK-STAT pathways (Takata et al 2021;Yao et al, 2021;Yunoki, 2018;Huang et al, 2020), other molecular mechanisms involved in the progression of eyelid BCC needs to be explored.…”

Section: Introductionmentioning

confidence: 99%

RBP1 promotes the progression of eyelid basal cell carcinoma via regulating OGN expression

Chen

Wang

et al. 2023

Preprint

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Objective Using RBP1 as the core gene to investigate the effects of RBP1 on the proliferation, migration and invasion of eyelid BCC cell line A431, and to explore its role in a mouse xenograft tumor model. To study in depth the specific molecular mechanisms by which RBP1 promotes the malignant progression of eyelid BCC, RNA-seq as well as bioinformatics analysis was performed to search for downstream genes with the aim of providing new potential targets for the treatment of eyelid BCC. Methods A sample of 30 patients with eyelid BCC who underwent surgery in the ophthalmology department of Huai'an First Hospital of Nanjing Medical University was selected. Protein mass spectrometry was used to examine three of the pairs of eyelid BCC cancer tissues and paracancerous tissues, and RBP1 was found to be highly expressed in eyelid BCC. The effect of RBP1 on eyelid BCC was investigated by clinical sample validation, in vitro cytology and mouse xenograft tumor model, and the downstream gene osteoglycin (OGN) was further screened by RNA-seq technology to verify that RBP1 can be involved in eyelid BCC progression by regulating OGN levels. Results The results showed that RBP1 was significantly more expressed in eyelid BCC tissues than in paracancerous tissues, and cellular experiments confirmed that RBP1 promoted proliferation, migration and invasion of eyelid BCC cells, and a mouse xenograft tumor model revealed that the gene could promote the growth of cancerous species. Meanwhile, salvage experiments showed that RBP1 accelerated the proliferation, migration, invasion and tumor growth of eyelid BCC cells in nude mice by suppressing OGN protein levels. Conclusion RBP1 was significantly upregulated in eyelid BCC. Interfering with RBP1 not only inhibited the proliferation, migration and invasion of A431 cells, but also inhibited the growth of transplanted tumors in nude mice. In addition, knockdown of OGN reversed the inhibitory effects of RBP1 interference on cell proliferation, migration and invasion. In summary, RBP1 can promote tumor progression in eyelid BCC by inhibiting OGN expression, which provides a new potential target for the treatment of eyelid BCC.

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Section: Introductionmentioning

confidence: 99%