研究证实，丙状口炎单胞菌（Pg）的定植可以促进食管鳞状细胞癌（ESCC）的恶性演化。由于致病微生物可以通过抑制程序性细胞死亡因子4（PDCD4）来促进恶性肿瘤增殖，而PDCD4活性的降低可以增强癌细胞的干细胞特性，因此我们在此研究中探讨了Pg通过抑制PDCD4和富集癌干细胞（CSCs）来促进ESCC化疗抵抗和恶性的功能机制。通过体外研究评估了Pg和PDCD4对ESCC细胞的CSCs、化疗抵抗性和恶性的影响。采用免疫组化检测了ESCC组织中的Pg、PDCD4和ALDH1的表达，并分析了每个指标与术后生存率的相关性。结果显示，Pg能够抑制PDCD4的表达并导致ESCC细胞中CSCs的富集。在消除Pg后，PDCD4的表达上调，CSCs的百分比、化疗抵抗性和恶性降低。具有Pg-阳性、PDCD4-阴性和ALDH1-阳性的ESCC患者的存活期明显较短。本研究证明，通过消除Pg和阻断PDCD4活性降低引起的CSCs富集，可能为ESCC治疗提供新策略。

Studies have confirmed that the colonization of Porphyromonas gingivalis (Pg) could promote the malignant evolution of esophageal squamous cell carcinoma (ESCC). Since pathogenic microorganisms can promote malignant tumor proliferation by inhibiting programmed cell death factor 4 (PDCD4) and the decrease of PDCD4 activity can enhance the stemness of cancer cells, we here investigated the functional mechanism by which Pg promoted ESCC chemoresistance and malignancy through inhibiting PDCD4 and enriching cancer stem cells (CSCs). The effects of Pg and PDCD4 on CSCs, chemoresistance and malignancy of ESCC cells were evaluated by in vitro studies. The expression of Pg, PDCD4, and ALDH1 in ESCC tissues were detected by IHC, and the correlations between each index and postoperative survival of ESCC patients were analyzed. The results showed that Pg could inhibit PDCD4 expression and lead to CSCs enrichment in ESCC cells. After eliminating Pg, the expression of PDCD4 was upregulated, the percentage of CSCs, chemoresistance and malignancy were decreased. ESCC patients with Pg-positive, PDCD4-negative, and ALDH1-positive have a significant shorter survival. This study proved that eliminating Pg and blocking CSCs enrichment caused by decreasing PDCD4 activity may provide a new strategy for ESCC treatment.