Kataoka Kozo, Fujimoto Koji, Ito Daisuke, Koizumi Masayuki, Toyoda Eiji, Mori Tomohiko, Kami Kazuhiro, Doi Ryuichiro
Department of Surgery and Basic Surgical Science, Kyoto University, Japan.
Surgery. 2005 Sep;138(3):450-5. doi: 10.1016/j.surg.2005.06.028.
Tuberous sclerosis complex (TSC) is an autosomal dominant disorder caused by mutation of either of 2 tumor suppressor genes, TSC1 or TSC2, which encode hamartin and tuberin, respectively. Several studies have shown that tuberin functions independently of hamartin and inhibits signaling pathways via the mammalian target of rapamycin, a critical regulator of cell proliferation. Recent studies have revealed that the signaling pathways regulating the mammalian target of rapamycin such as Akt and S6K1 are frequently activated in pancreatic cancer. We hypothesized that tuberin might be involved in the proliferation and survival of pancreatic cancer cells.
We immunohistochemically examined the expression of tuberin in 42 pancreatic cancerous and noncancerous pancreatic tissue specimens using an antituberin antibody. The correlations between tuberin expression and various clinicopathologic features, including survival, were evaluated. Reverse transcriptase-polymerase chain reaction was performed to evaluate the level of tuberin expression in paired samples of pancreatic cancer and noncancerous tissue.
Twenty-four of the 42 pancreatic cancer samples (57%) were negative for tuberin expression. The patients with tuberin-negative tumors had a significantly higher incidence of pT3 or pT4 disease (primary tumor extent by the TNM classification) than those with tuberin-positive tumors (P = .024). Female patients had a significantly higher incidence of tuberin-positive tumors than male patients (P = .014). The survival rate of the tuberin-positive group tended to be better than that of the tuberin-negative group, but there was no significant difference (P = .4). Expression of TSC2 in cancer tissue was lower than in the corresponding noncancerous tissue for 7 of the 9 samples examined.
This study demonstrates that reduced expression of tuberin might be involved in the progression of pancreatic cancer. Accordingly, tuberin may provide a new therapeutic target in patients with this type of cancer.
结节性硬化症(TSC)是一种常染色体显性疾病,由两个肿瘤抑制基因TSC1或TSC2中的任一个发生突变引起,这两个基因分别编码错构瘤蛋白和结节蛋白。多项研究表明,结节蛋白独立于错构瘤蛋白发挥作用,并通过哺乳动物雷帕霉素靶蛋白(细胞增殖的关键调节因子)抑制信号通路。最近的研究显示,调节哺乳动物雷帕霉素靶蛋白的信号通路,如Akt和S6K1,在胰腺癌中经常被激活。我们推测结节蛋白可能参与胰腺癌细胞的增殖和存活。
我们使用抗结节蛋白抗体,对42份胰腺癌组织和非癌性胰腺组织标本进行免疫组织化学检测,以检查结节蛋白的表达情况。评估结节蛋白表达与各种临床病理特征(包括生存率)之间的相关性。进行逆转录聚合酶链反应,以评估胰腺癌组织和非癌性组织配对样本中结节蛋白的表达水平。
42份胰腺癌样本中有24份(57%)结节蛋白表达呈阴性。结节蛋白阴性肿瘤患者的pT3或pT4疾病(根据TNM分类的原发肿瘤范围)发生率显著高于结节蛋白阳性肿瘤患者(P = 0.024)。女性患者结节蛋白阳性肿瘤的发生率显著高于男性患者(P = 0.014)。结节蛋白阳性组的生存率倾向于高于结节蛋白阴性组,但差异无统计学意义(P = 0.4)。在所检测的9份样本中,有7份样本的癌组织中TSC2的表达低于相应的非癌性组织。
本研究表明,结节蛋白表达降低可能参与胰腺癌的进展。因此,结节蛋白可能为这类癌症患者提供一个新的治疗靶点。