Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, Linköping, Sweden.
Radiol Oncol. 2011 Dec;45(4):279-84. doi: 10.2478/v10019-011-0030-7. Epub 2011 Sep 22.
In the present study, we investigated NF-κB p65 phosphorylated at Serine-536 (phosphor-Ser536-p65) in rectal cancer and its relationship to preoperative radiotherapy (RT), clinicopathological variables and biological factors.
Expression of phosphor-Ser536-p65 was examined by using immunohistochemistry in 141 primary rectal cancers, 149 normal mucosa specimens and 48 metastases in the lymph nodes, from rectal cancer patients who participated in a Swedish clinical trial of preoperative RT.
The expression of phosphor-Ser536-p65 in the cytoplasm increased from normal mucosa to primary tumour (p<0.0001, for both the group that did and the group that did not received RT). The expression did not further increase from primary tumour to metastasis in either group (p>0.05). Expression of phosphor-Ser536-p65 was positively related to, or tended to be related to, the expression of tumour endothelium marker 1 (TEM1, p=0.02), FXYD-3 (p=0.001), phosphatase of regenerating liver (PRL, p=0.02), p73 (p=0.048) and meningioma associated protein (MAC30, p=0.05) in the group that received RT but there were no such relationships in the group that did not received RT (p>0.05). The expression of phosphor-Ser536-p65 was not related to clinicopathological factors including survival (p>0.05).
The increased expression of phosphor-Ser536-p65 may be involved in rectal cancer development. After RT, phosphor-Ser536-p65 seems to be positively related to the biological factors, which associated with more malignant features of tumours. However, phosphor-Ser536-p65 was not directly related to the response of RT based on recurrence and survival.
在本研究中，我们研究了直肠癌中 NF-κB p65 丝氨酸-536 磷酸化（磷酸化 Ser536-p65）及其与术前放疗（RT）、临床病理变量和生物学因素的关系。
使用免疫组织化学法检测了 141 例直肠癌、149 例正常直肠黏膜标本和 48 例淋巴结转移患者的磷酸化 Ser536-p65 表达，这些患者均来自参加瑞典术前 RT 临床研究的直肠癌患者。
细胞质中磷酸化 Ser536-p65 的表达从正常黏膜到原发性肿瘤逐渐增加（两组均有 p<0.0001，均接受 RT）。在两组中，从原发性肿瘤到转移瘤的表达均未进一步增加（p>0.05）。磷酸化 Ser536-p65 的表达与肿瘤内皮标志物 1（TEM1，p=0.02）、FXYD-3（p=0.001）、肝再生磷酸酶（PRL，p=0.02）、p73（p=0.048）和脑膜瘤相关蛋白（MAC30，p=0.05）的表达呈正相关，或有相关趋势在接受 RT 的组中，但在未接受 RT 的组中无相关关系（p>0.05）。磷酸化 Ser536-p65 的表达与包括生存在内的临床病理因素无关（p>0.05）。
磷酸化 Ser536-p65 的表达增加可能参与直肠癌的发生。在 RT 后，磷酸化 Ser536-p65 似乎与生物学因素呈正相关，这些因素与肿瘤更恶性的特征相关。然而，磷酸化 Ser536-p65 与基于复发和生存的 RT 反应并无直接关系。
