Oral squamous cell carcinoma (OSCC) is a prevalent and significant type of oral cancer that has far-reaching health implications worldwide. Epigenetics, a field focused on studying heritable changes in gene expression without modifying DNA sequence, plays a pivotal role in OSCC. Epigenetic changes, encompassing DNA methylation, histone modifications, and miRNAs, exert control over gene activity and cellular characteristics. In OSCC, aberrant DNA methylation of tumor suppressor genes (TSG) leads to their inactivation, subsequently facilitating tumor growth. As a result, distinct patterns of gene methylation hold promise as valuable biomarkers for the detection of OSCC. Oral cancer treatment typically involves surgery, radiation therapy, and chemotherapy, but even with these treatments, cancer cells cannot be effectively targeted and destroyed. Researchers are therefore exploring new methods to target and eliminate cancer cells. One promising approach is the use of epigenetic modifiers, such as DNA methyltransferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibitors, which have been shown to modify abnormal epigenetic patterns in OSCC cells, leading to the reactivation of TSGs and the suppression of oncogenes. As a result, epigenetic-targeted therapies have the potential to directly alter gene expression and minimize side effects. Several studies have explored the efficacy of such therapies in the treatment of OSCC. Although studies have investigated the efficacy of epigenetic therapies, challenges in identifying reliable biomarkers and developing effective combination treatments are acknowledged. Of note, epigenetic mechanisms play a significant role in drug resistance in OSCC and other cancers. Aberrant DNA methylation can silence tumor suppressor genes, while alterations in histone modifications and chromatin remodeling affect gene expression related to drug metabolism and cell survival. Thus, understanding and targeting these epigenetic processes offer potential strategies to overcome drug resistance and improve the efficacy of cancer treatments in OSCC. This comprehensive review focuses on the complex interplay between epigenetic alterations and OSCC cells. This will involve a deep dive into the mechanisms underlying epigenetic modifications and their impact on OSCC, including its initiation, progression, and metastasis. Furthermore, this review will present the role of epigenetics in the treatment and diagnosis of OSCC.
口腔鳞状细胞癌（OSCC）是一种常见且重要的口腔癌类型，在全球范围内具有深远的健康影响。表观遗传学作为研究不改变DNA序列的可遗传基因表达变化的领域，在OSCC中起着关键作用。表观遗传变化包括DNA甲基化、组蛋白修饰和miRNA，这些变化控制着基因活性和细胞特性。在OSCC中，肿瘤抑制基因（TSG）的异常DNA甲基化导致其失活，进而促进肿瘤生长。因此，特定的基因甲基化模式有望成为检测OSCC的有价值的生物标志物。 口腔癌的治疗通常包括手术、放疗和化疗，但即使采用这些治疗方法，癌细胞仍无法被有效靶向和清除。因此，研究人员正在探索靶向和清除癌细胞的新方法。一种有前景的方法是使用表观遗传修饰剂，如DNA甲基转移酶（DNMT）抑制剂和组蛋白去乙酰化酶（HDAC）抑制剂。这些抑制剂已被证明可以改变OSCC细胞中的异常表观遗传模式，从而重新激活TSG并抑制癌基因。因此，表观遗传靶向治疗具有直接改变基因表达并减少副作用的潜力。多项研究已探讨了此类疗法在OSCC治疗中的效果。 尽管已有研究探讨了表观遗传疗法的效果，但识别可靠的生物标志物和开发有效的联合治疗方案仍面临挑战。值得注意的是，表观遗传机制在OSCC及其他癌症的耐药性中起着重要作用。异常的DNA甲基化可能导致肿瘤抑制基因沉默，而组蛋白修饰和染色质重塑的改变则会影响与药物代谢和细胞存活相关的基因表达。因此，理解和靶向这些表观遗传过程为克服耐药性、提高OSCC癌症治疗效果提供了潜在策略。 本综述重点关注表观遗传改变与OSCC细胞之间的复杂相互作用，深入探讨表观遗传修饰的机制及其对OSCC发生、发展和转移的影响。此外，本文还将阐述表观遗传学在OSCC治疗和诊断中的作用。
Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review
肿瘤(癌症)患者之家