Letters to editor regarding the article "P4HA2 contributes to head and neck squamous cell carcinoma progression and EMT through PI3K/AKT signaling pathway".

IF 2.8 4区 医学 Q2 ONCOLOGY Medical Oncology Pub Date : 2024-08-13 DOI:10.1007/s12032-024-02436-z
K L G Afeeza, S Balachandran, S Muthamizh, E Dilipan
{"title":"Letters to editor regarding the article \"P4HA2 contributes to head and neck squamous cell carcinoma progression and EMT through PI3K/AKT signaling pathway\".","authors":"K L G Afeeza, S Balachandran, S Muthamizh, E Dilipan","doi":"10.1007/s12032-024-02436-z","DOIUrl":null,"url":null,"abstract":"<p><p>We have read the original article titled \"P4HA2 contributes to head and neck squamous carcinoma progression and EMT through PI3K/AKT signaling pathway\" by Yan-Ling Wu et al., which was published in the Medical Oncology journal, with great interest. This study provides valuable insights into the involvement of P4HA2 in the progression of head and neck squamous cell carcinoma (HNSCC), highlighting its potential as an oncogenic factor that promotes epithelial-mesenchymal transition (EMT), motility, invasion, and proliferation of cancer cells through the PI3K/AKT signaling pathway. While this work enhances our understanding of the role of P4HA2 in HNSCC, there are certain aspects that remain unexplored. These areas could be further investigated in future research to obtain a more comprehensive understanding. Specifically, the study did not investigate other signaling pathways or molecular mechanisms through which P4HA2 may impact the development of HNSCC. By exploring these molecular pathways, it may be possible to identify specific targets for pharmaceutical intervention to inhibit the production of P4HA2. Examining these aspects in future research would significantly contribute to our understanding of the role of P4HA2 in HNSCC and its potential as a therapeutic target. We appreciate the authors for their significant contribution and eagerly await future studies that expand upon these findings.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"41 9","pages":"225"},"PeriodicalIF":2.8000,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12032-024-02436-z","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

We have read the original article titled "P4HA2 contributes to head and neck squamous carcinoma progression and EMT through PI3K/AKT signaling pathway" by Yan-Ling Wu et al., which was published in the Medical Oncology journal, with great interest. This study provides valuable insights into the involvement of P4HA2 in the progression of head and neck squamous cell carcinoma (HNSCC), highlighting its potential as an oncogenic factor that promotes epithelial-mesenchymal transition (EMT), motility, invasion, and proliferation of cancer cells through the PI3K/AKT signaling pathway. While this work enhances our understanding of the role of P4HA2 in HNSCC, there are certain aspects that remain unexplored. These areas could be further investigated in future research to obtain a more comprehensive understanding. Specifically, the study did not investigate other signaling pathways or molecular mechanisms through which P4HA2 may impact the development of HNSCC. By exploring these molecular pathways, it may be possible to identify specific targets for pharmaceutical intervention to inhibit the production of P4HA2. Examining these aspects in future research would significantly contribute to our understanding of the role of P4HA2 in HNSCC and its potential as a therapeutic target. We appreciate the authors for their significant contribution and eagerly await future studies that expand upon these findings.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
致编辑的信,内容涉及文章 "P4HA2通过PI3K/AKT信号通路促进头颈部鳞状细胞癌的进展和EMT"。
我们饶有兴趣地阅读了吴艳玲等人发表在《肿瘤内科学》(Medical Oncology)杂志上的题为《P4HA2 contributes to head and neck squamous carcinoma progression and EMT through PI3K/AKT signaling pathway》的原创文章。这项研究就 P4HA2 参与头颈部鳞状细胞癌(HNSCC)的进展提供了有价值的见解,突出了其作为致癌因子的潜力,它通过 PI3K/AKT 信号通路促进上皮-间质转化(EMT)、运动、侵袭和癌细胞增殖。虽然这项研究加深了我们对 P4HA2 在 HNSCC 中作用的了解,但仍有某些方面有待探索。这些方面可在今后的研究中进一步探究,以获得更全面的认识。具体来说,该研究没有调查 P4HA2 可能影响 HNSCC 发展的其他信号通路或分子机制。通过探索这些分子途径,也许可以确定药物干预的特定靶点,以抑制 P4HA2 的产生。在未来的研究中探讨这些方面将大大有助于我们了解 P4HA2 在 HNSCC 中的作用及其作为治疗靶点的潜力。我们感谢作者们的重大贡献,并热切期待未来的研究能进一步拓展这些发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Medical Oncology
Medical Oncology 医学-肿瘤学
CiteScore
4.20
自引率
2.90%
发文量
259
审稿时长
1.4 months
期刊介绍: Medical Oncology (MO) communicates the results of clinical and experimental research in oncology and hematology, particularly experimental therapeutics within the fields of immunotherapy and chemotherapy. It also provides state-of-the-art reviews on clinical and experimental therapies. Topics covered include immunobiology, pathogenesis, and treatment of malignant tumors.
期刊最新文献
Dual roles of extracellular vesicles in acute lymphoblastic leukemia: implications for disease progression and theranostic strategies. Letter to the editor: the potential value of NDUFA4L2 in colon adenocarcinoma remains to be fully evaluated. Targeting the mevalonate pathway enhances the efficacy of 5-fluorouracil by regulating pyroptosis. Red wavelength-induced photobiomodulation enhances indocyanine green-based anticancer photodynamic therapy. Thapsigargin and its prodrug derivatives: exploring novel approaches for targeted cancer therapy through calcium signaling disruption.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1