Placenta‑specific protein 1 (PLAC1) is inversely associated with survival in several types of cancer. However, whether PLAC1 is involved in the progression of cervical cancer (CC) remains to be elucidated. Therefore, the present study aimed to evaluate the prognostic role of PLAC1 in CC by determining the relationship between clinicopathological factors, PLAC1 gene expression and survival prognosis using univariate and multivariate Cox proportional‑hazards regression analyses. Similarly, Kaplan‑Meier curves were evaluated with the log‑rank test. Subsequently, gene set enrichment analysis was performed to compare the high‑ and low‑PLAC1 expression phenotypes. Functional studies were further conducted in PLAC1‑overexpressing HeLa cells and PLAC1‑silenced MS751 cells, and western blotting was performed to determine whether PLAC1 promoted CC progression via epithelial‑mesenchymal transition (EMT). The findings demonstrated that high expression of PLAC1 was associated with American Joint Committee on Cancer metastasis pathological score and suggested a poor overall survival. 'mTOR complex 1 signaling', 'interferon α response' and 'hypoxia' were differentially enriched in the high‑PLAC1 phenotype. Furthermore, PLAC1 promoted the invasion of CC cells in vitro. E‑cadherin expression was decreased in the PLAC1‑overexpressing cells, accompanied by increased expression of the mesenchymal markers, Vimentin, MMP2 and Slug, and the opposite effects were observed in PLAC1‑silenced cells. Taken together, the present results indicated that high expression of PLAC1 was associated with poor survival and PLAC1 promoted metastasis via EMT in CC.

中文翻译：

---

PLAC1 是不良生存率的独立预测因子，可促进宫颈癌的细胞增殖和侵袭。

胎盘特异性蛋白 1 (PLAC1) 与几种癌症的存活率呈负相关。然而，PLAC1是否参与宫颈癌（CC）的进展仍有待阐明。因此，本研究旨在通过确定临床病理因素与PLAC1之间的关系来评估 PLAC1 在 CC 中的预后作用。使用单变量和多变量 Cox 比例风险回归分析的基因表达和生存预后。同样，使用对数秩检验评估 Kaplan-Meier 曲线。随后，进行基因集富集分析以比较高和低 PLAC1 表达表型。在 PLAC1 过表达的 HeLa 细胞和 PLAC1 沉默的 MS751 细胞中进一步进行了功能研究，并进行了蛋白质印迹以确定 PLAC1 是否通过上皮间质转化 (EMT) 促进 CC 进展。研究结果表明，PLAC1 的高表达与美国癌症转移联合委员会病理评分相关，并表明总体生存率较差。“mTOR 复合物 1 信号”、“干扰素 α 反应”和“缺氧” 在高PLAC1表型中差异富集。此外，PLAC1促进CC细胞的侵袭体外。E-cadherin 在 PLAC1 过表达细胞中的表达降低，伴随着间充质标志物 Vimentin、MMP2 和 Slug 的表达增加，而在 PLAC1 沉默的细胞中观察到相反的效果。总之，目前的结果表明 PLAC1 的高表达与较差的存活率相关，并且 PLAC1 通过 EMT 在 CC 中促进转移。