Background

Human endogenous retrovirus (HERV)-K is a type of retrovirus that is present in the human genome, and its expression is usually silenced in healthy tissues. The precise mechanism by which HERV-K env influences cancer stemness is not fully understood, but it has been suggested that HERV-K env may activate various signaling pathways that promote stemness traits in cancer cells.

Objective

To establish the connection between HERV-K env expression and cancer stemness in ovarian cancer cells, we carried out correlation analyses between HERV-K env and the cancer stem cell (CSC) marker known as the cluster of differentiation 133 (CD133) gene in SKOV3 ovarian cancer cells.

Method

To perform correlation analysis between HERV-K env and CSCs, ovarian cancer cells were cultured in a medium designed for cancer stem cell induction. The expression of HERV-K env and CD133 genes was verified using quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot analyses. Additionally, the expression of stemness-related markers, such as OCT-4 and Nanog, was also confirmed using RT-qPCR.

Results

In the stem cell induction medium, the number of tumorsphere-type SKOV3 cells increased, and the expression of CD133 and HERV-K env genes was up-regulated. Additionally, other stemness-related markers like OCT-4 and Nanog also exhibited increased expression when cultured in the cancer stem cell induction medium. However, when HERV-K env knockout (KO) SKOV3 cells were cultured in the same cancer stem cell induction medium, there was a significant decrease in the number of tumorsphere-type cells compared to mock SKOV3 cells subjected to the same conditions. Furthermore, the expression of CD133, Nanog, and OCT-4 did not show a significant increase in HERV-K env KO SKOV3 cells compared to mock SKOV3 cells cultured in the same cancer stem cell induction medium.

Conclusion

These findings indicate that the expression of HERV-K env increased in SKOV3 cells when cultured in cancer stem cell induction media, and cancer stem cell induction was inhibited by KO of HERV-K env in SKOV3 cells. These results suggest a strong association between HERV-K env and stemness in SKOV3 ovarian cancer cells.

中文翻译：

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SKOV3卵巢癌细胞中肿瘤干细胞标志物CD133与人内源性逆转录病毒（HERV）-K env的相关性分析

背景

人内源性逆转录病毒（HERV）-K是一种存在于人类基因组中的逆转录病毒，其表达通常在健康组织中沉默。 HERV-K env影响癌症干性的确切机制尚不完全清楚，但有人认为 HERV-K env可能激活各种信号通路，促进癌细胞的干性特征。

客观的

为了建立卵巢癌细胞中HERV-K env表达与癌症干性之间的联系，我们对 SKOV3 中 HERV-K env与癌症干细胞 (CSC) 标记（称为分化簇 133 ( CD133 ) 基因）之间进行了相关性分析。卵巢癌细胞。

方法

为了进行 HERV-K env和 CSC 之间的相关性分析，在专为癌症干细胞诱导设计的培养基中培养卵巢癌细胞。使用定量实时聚合酶链反应 (RT-qPCR) 和蛋白质印迹分析验证HERV-K env和CD133基因的表达。此外，还使用 ​​RT-qPCR 证实了干性相关标记的表达，例如OCT-4和Nanog。

结果

在干细胞诱导培养基中，肿瘤球型SKOV3细胞数量增加，CD133和HERV-K env基因表达上调。此外，在癌症干细胞诱导培养基中培养时，其他干性相关标记物（如OCT-4和Nanog）也表现出表达增加。然而，当HERV-K env敲除（KO）SKOV3细胞在相同的癌症干细胞诱导培养基中培养时，与相同条件下的模拟SKOV3细胞相比，肿瘤球型细胞的数量显着减少。此外，与在相同癌症干细胞诱导培养基中培养的模拟SKOV3细胞相比， HERV-K env KO SKOV3细胞中CD133、Nanog和OCT-4的表达没有显示出显着增加。

结论

这些发现表明，当在癌症干细胞诱导培养基中培养时，SKOV3细胞中HERV-K env的表达增加，并且SKOV3细胞中HERV-K env的KO抑制了癌症干细胞诱导。这些结果表明SKOV3 卵巢癌细胞中HERV-K env与干性之间存在密切相关。