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肿瘤相关抗原RCAS1在口腔鳞状细胞癌中的表达及其可能参与免疫逃逸的机制

Expression of tumor-associated antigen RCAS1 and its possible involvement in immune evasion in oral squamous cell carcinoma.

作者信息

Toyoshima T, Nakamura S, Kumamaru W, Kawamura E, Ishibashi H, Hayashida J-N, Moriyama M, Ohyama Y, Sasaki M, Shirasuna K

机构信息

Section of Oral and Maxillofacial Surgery, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.

出版信息

J Oral Pathol Med. 2006 Jul;35(6):361-8. doi: 10.1111/j.1600-0714.2006.00442.x.

Abstract

BACKGROUND

RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is known to induce apoptosis in its receptor-positive cells. The authors investigated RCAS1 expression in oral squamous cell carcinoma (SCC) and its association with the apoptosis of tumor-infiltrating lymphocytes (TILs).

METHODS

In 130 patients with oral SCC, the expression of RCAS1 in tumor cells was immunohistochemically examined and the apoptosis of TILs was examined by Terminal Deoxynucleotidyltransferase-mediated dUTP Nick End Labeling (TUNEL) staining.

RESULTS

RCAS1 was detected both on the cytoplasm and the membrane of tumor cells in 41 of 130 cases (31.5%). Focusing on the expression at the invasive front interacting with host immune cells, RCAS1 was detected in 22 of 130 cases (16.9%). The percentage of TUNEL-positive TILs in cases with RCAS1-positive SCCs was significantly higher than in cases with RCAS1-negative SCCs (P < 0.0001).

CONCLUSIONS

RCAS1 can be expressed on oral SCC cells and may be involved in the tumor escape from the host immune system by inducing the apoptosis of TILs.

摘要

背景

已知RCAS1(SiSo细胞上表达的受体结合癌抗原)可诱导其受体阳性细胞发生凋亡。作者研究了口腔鳞状细胞癌(SCC)中RCAS1的表达及其与肿瘤浸润淋巴细胞(TILs)凋亡的关系。

方法

对130例口腔SCC患者,采用免疫组织化学方法检测肿瘤细胞中RCAS1的表达,并用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测TILs的凋亡情况。

结果

130例中有41例(31.5%)肿瘤细胞的细胞质和细胞膜上均检测到RCAS1。聚焦于与宿主免疫细胞相互作用的浸润前沿的表达,130例中有22例(16.9%)检测到RCAS1。RCAS1阳性SCC病例中TUNEL阳性TILs的百分比显著高于RCAS1阴性SCC病例(P < 0.0001)。

结论

RCAS1可在口腔SCC细胞上表达,并可能通过诱导TILs凋亡参与肿瘤逃避宿主免疫系统的过程。

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