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The study investigates FAM111B, previously linked to LUAD, showing pan-cancer evidence of high expression and an oncogenic role in LUSC. Using in vitro and in vivo FAM111B knockdown models, the work demonstrates reduced proliferation, migration, and invasion, S-phase cell-cycle arrest, and PI3K-related EMT-associated mechanisms, supporting therapeutic target potential.",{"@graph":69,"@context":114},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/fam111b-may-promote-the-progression-of-lung-squamous-cell-carcinoma-through-pi3k-signaling-pathway/350660/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/fam111b-may-promote-the-progression-of-lung-squamous-cell-carcinoma-through-pi3k-signaling-pathway/350660.png","ImageObject",300,407,{"name":92,"@type":93},"kopisore","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-25","2026-09-22",true,{"@type":102,"interactionType":103,"userInteractionCount":14},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108],{"name":109,"@type":110,"acceptedAnswer":111},"What mechanism links FAM111B to increased migration and invasion in LUSC?","Question",{"text":112,"@type":113},"FAM111B facilitates epithelial-mesenchymal transition (EMT), supporting enhanced migration and invasion. The study also connects proliferation and cell-cycle processes to the PI3K signaling pathway.","Answer","https://schema.org",{"og:url":83,"og:type":116,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":118,"canonical":83},"index,follow",{"doc_id":120,"site_id":62},350660,1790379899,{"code":4,"msg":5,"data":123},{"doc_id":120,"user_id":124,"nickname":92,"user_avatar":125,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":126,"file_id":127,"file_url":128,"file_type":129,"file_size":130,"view_count":14,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":131,"language":132,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":133,"faqs":134,"seo_title":135,"seo_description":67,"update_tm":136,"read_time":137},962090880963,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nFAM111B may promote the progression of lung squamous cell carcinoma through PI3K signaling pathway  \nYajuan Chen1,5, Shiwei Chai4,5, Huimin Wang2, Yunyi Chen1, Yanting Bi1, Yifei Ma1, Ruotian Li1, Ruiyi Liu1, Zaoxiu Hu3􀀍 & Shaoxiang Wan2􀀍  \nLung squamous cell carcinoma (LUSC) is a subtype of non-small cell lung cancer (NSCLC) . Compared to lung adenocarcinoma (LUAD), LUSC is characterized by a greater propensity for recurrence and metastasis, poorer prognosis, and shorter survival. Therefore, further research into the pathogenesis of LUSC and the identification of new therapeutic targets are essential to advance clinical treatment options for this aggressive cancer. FAM111B, a serine protease and cancer-associated nuclear protein, has been implicated in various cancers. Previous studies have shown that FAM111B is closely associated with the progression of LUAD. However, our pan-cancer analysis suggests that FAM111B is highly expressed in LUSC and plays an oncogenic role, which is consistent with its higher expression in LUSC compared to LUAD in clinical samples. To investigate the functional role of FAM111B in LUSC, we developed both in vitro and in vivo knockdown models. Our results demonstrate that knocking down FAM111B significantly inhibits the proliferation, migration, and invasion of LUSC cells. Additionally, FAM111B knockdown induces cell cycle arrest in the S phase, further underscoring its role in LUSC progression. Mechanistically, FAM111B promotes LUSC migration and invasion by facilitating epithelial-mesenchymal transition (EMT) . Moreover, the proliferation and cell cycle processes in LUSC may be regulated through the PI3K signaling pathway. In conclusion, our study elucidates the clinical relevance and molecular mechanisms of FAM111B in LUSC, highlighting its potential as a novel therapeutic target for this challenging cancer subtype.  \nKeywords Lung squamous cell carcinoma, FAM111B, PI3K  \nAccording to Globocan 2024, lung cancer remains the deadliest cancer in the world1. Lung cancer can be roughly divided into small cell lung cancer (SCLC) and non-SCLC (NSCLC) according to histology, accounting for about 85% and 15% of the total number of lung cancer, respectively2. NSCLC can be divided into lung squamous cell carcinoma (LUSC), lung adenocarcinoma (LUAD), and large cell carcinoma (LCC), and LUSC accounts for about 30% of NSCLC patients3. Compared with LUAD, LUSC has a high incidence, strong drug resistance, easy recurrence and metastasis, poor prognosis, short survival, and a lack of early diagnosis and treatment strategies4,5.  \nChemotherapy still plays an irreplaceable role in the treatment ofLUSC, but its specificity is poor. In addition to chemotherapy, immunotherapy, and targeted therapies, lung cancer can benefit cancer patients. EGFR-TKIis still the main target therapy for advanced LUSC in the world, such as erlotinib and afatinib6. However, the common gene mutations in LUAD, such as EGFR and KRAS, are rarely mutated in LUSC, so LUSC patients find it difficult to benefit from EGFR inhibitors7. The frequency of total gene mutations in patients with LUSCis high and complex, and targeted therapies for LUSC are still being explored. Many new drugs in patients with  \n1Yunnan Key Laboratory of Breast Cancer Precision Medicine, Academy of Biomedical Engineering, Kunming Medical University, Kunming 650500, Yunnan, P. R. China. 2Department of Pharmacy, Yunnan Provincial Hospital of Infectious Diseases/Yunnan AIDS Care Center, 28 km from Anning Shi’an Road, Kunming 650399, Yunnan, P.R. China. 3Department of Pathology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, 519 Kunzhou Road, Xishan District, Kunming 650118, Yunnan, P. R. China. 4Zhanjiang Health School of Guangdong, Zhanjiang 524094, Guangdong, P. R. China. 5Yajuan Chen and Shiwei Chai contributed equally to this work. 􀀍 email: [1046464409@qq","cbCaicSpOcDRYG4n","https://ap.wps.com/l/cbCaicSpOcDRYG4n","pdf",4631310,17,"English","# Background\n## Lung squamous cell carcinoma and unmet needs\n## FAM111B and PI3K signaling rationale\n# Methods\n## In vitro and in vivo knockdown models\n# Results\n## Effects on proliferation, migration, and invasion\n## Cell cycle arrest in S phase\n## EMT and PI3K pathway mechanism\n# Conclusion","[{\"question\":\"What mechanism links FAM111B to increased migration and invasion in LUSC?\",\"answer\":\"FAM111B facilitates epithelial-mesenchymal transition (EMT), supporting enhanced migration and invasion. The study also connects proliferation and cell-cycle processes to the PI3K signaling pathway.\"}]","FAM111B may promote the progression of lung squamous cell carcinoma through PI3K signaling pathway | PDF",1790090463,43]