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【medical-news】转移性乳腺癌的关键机制确定

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转移性乳腺癌的关键机制确定
Key Mechanism Identified in Metastatic Breast Cancer
原文：
ScienceDaily (May 4, 2010) — Scientists at the University of Kentucky Markey Cancer Center have identified a key molecular mechanism in breast cancer that enables tumor cells to spread to adjacent or distant parts of the body in a process called metastasis. This finding opens the way to new lines of research aimed at developing treatments for metastatic breast cancer.
The research, led by Peter Zhou, associate professor of molecular and cellular biochemistry at UK, focused on the process by which tumor cells stop clinging to other cells and become motile, or able to spread throughout the body. The findings were published in an article in the EMBO Journal, the flagship publication of the European Molecular Biology Organization.
The increased motility of tumor cells at the initial step of metastasis is similar to a process called epithelial-mesenchymal transition (EMT), which is required for large-scale cell movement in embryonic development, tissue remodeling and wound healing. For example, during wound healing, cells at the edge of the wound undergo a EMT process and migrate to the middle for sealing the wound.
In all EMT processes, cells lose the expression of a cell-to-cell adhesion molecule called E-cadherin, which functions as a "molecular glue" that attaches cells to one another. Breast cancer cells usurp this process for invasion and metastasis. When this molecular glue is broken down, tumor cells start to migrate and spread throughout the body.
A protein called Snail acts as a master switch in the cell's nucleus to suppress E-cadherin expression and induce EMT in the cell. Previous research has shown Snail to be elevated in many types of cancer, particularly breast cancer. High levels of Snail have been linked to metastasis, tumor cell survival and tumor recurrence, and thus predict a poor clinical outcome for women with breast cancer. However, scientists are still not clear how Snail triggers the down-regulation of E-cadherin and induces metastasis in breast cancer.
Using a protein purification approach, Zhou and his colleagues found that Snail interacts and teams up with its "partner in crime," an enzyme called LSD1, inside the cell. LSD1 is known to change the structure of DNA and shut down the expression of many genes.
LSD1, which stands for lysine-specific demethylase-1 (and is chemically unrelated to the hallucinogen LSD), regulates the structure of the chromosome by removing a key methylation at histone H3, a core component that warps the DNA into compact conformation. This event triggers the "closure" of DNA structure and shuts down gene expression, such as E-cadherin. Zhou's team showed that the N-terminal portion of Snail molecular functions as a "molecular hook" for recruiting LSD1 to the E-cadherin gene, which, in turn, shuts down the expression of E-cadherin and induces tumor cell invasion and metastasis.
"This finding has significant clinical ramification, because chemical compounds or agents that can disrupt the interaction of Snail with LSD1 will have a great therapeutic potential of treating metastatic breast cancer," Zhou said. "Scientists at the Markey Cancer Center are currently exploring this idea and are keen to develop drugs that can treat metastatic cancer."
Breast cancer is the most common cancer in women. Approximately 90 percent of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells, and the average survival after documentation of metastasis is approximately two years.
"An understanding of the mechanism underlying the biology of breast cancer metastasis will provide novel therapeutic approaches to combat this life-threatening disease," Zhou said.

原文地址：http://www.sciencedaily.com/releases/2010/05/100504173825.htm

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2010-05-05 15:31 浏览 : 1116 回复 : 5

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本人认领该文，若48小时后未提交，请其他战友认领。

2010-05-06 19:58

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• 首套【肺石医生】表情上架啦，一起斗图吧！

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ScienceDaily (May 4, 2010) — Scientists at the University of Kentucky Markey Cancer Center have identified a key molecular mechanism in breast cancer that enables tumor cells to spread to adjacent or distant parts of the body in a process called metastasis. This finding opens the way to new lines of research aimed at developing treatments for metastatic breast cancer.
每日科学2010年5月4日报道，肯塔基大学Markey癌症中心的科学家们在乳腺癌中发现了一种能使肿瘤细胞向邻近或远处扩散的分子机制，该种过程被称为转移。该发现为针对转移性乳腺癌治疗进行一系列新的研究打开了道路。
The research, led by Peter Zhou, associate professor of molecular and cellular biochemistry at UK, focused on the process by which tumor cells stop clinging to other cells and become motile, or able to spread throughout the body. The findings were published in an article in the EMBO Journal, the flagship publication of the European Molecular Biology Organization.
由英国分子和细胞生物化学助教教授皮特.周领导的这项研究，主要集中研究肿瘤细胞停止粘附于其他细胞，变为可移动或能扩散到机体的过程。该项研究已论文的形式发表于EMBO杂志上，该杂志是欧洲分子生物学组织的旗舰出版物。
The increased motility of tumor cells at the initial step of metastasis is similar to a process called epithelial-mesenchymal transition (EMT), which is required for large-scale cell movement in embryonic development, tissue remodeling and wound healing. For example, during wound healing, cells at the edge of the wound undergo a EMT process and migrate to the middle for sealing the wound.
肿瘤细胞在转移开始阶段移动性增加类似于上皮-间质移行（EMT），而EMT是胚胎发育、组织重构和创伤愈合等所必需的。例如，在创伤愈合中，伤口边缘的细胞经历EMT过程并迁移到伤口中间而进行愈合。
In all EMT processes, cells lose the expression of a cell-to-cell adhesion molecule called E-cadherin, which functions as a "molecular glue" that attaches cells to one another. Breast cancer cells usurp this process for invasion and metastasis. When this molecular glue is broken down, tumor cells start to migrate and spread throughout the body.
在所有EMT过程中，细胞失去称为E-cadherin的细胞-细胞粘附分子的表达，其作为“分子胶水”将细胞互相粘附。乳腺癌细胞为了浸润和转移而可破坏这个过程。当分子胶水被破坏了，肿瘤细胞开始迁移并扩散到机体。
A protein called Snail acts as a master switch in the cell's nucleus to suppress E-cadherin expression and induce EMT in the cell. Previous research has shown Snail to be elevated in many types of cancer, particularly breast cancer. High levels of Snail have been linked to metastasis, tumor cell survival and tumor recurrence, and thus predict a poor clinical outcome for women with breast cancer. However, scientists are still not clear how Snail triggers the down-regulation of E-cadherin and induces metastasis in breast cancer.
Snail蛋白作为总开关在细胞核内科抑制E-cadherin的表达和诱导EMT发生。以前的研究显示snail在许多类型癌特别是乳腺癌中增高。Snail表达增高与转移、肿瘤细胞生存和肿瘤复发密切相关，因此可预测乳腺癌病人具有较差的临床结局。然而，科学家们还不清楚snail是如何启动E-cadherin下调和诱导乳腺癌转移的。
Using a protein purification approach, Zhou and his colleagues found that Snail interacts and teams up with its "partner in crime," an enzyme called LSD1, inside the cell. LSD1 is known to change the structure of DNA and shut down the expression of many genes.
使用蛋白纯化技术，周和其同事发现了snail与其“罪犯伙伴”，一种称为LSD1的酶相互作用并组成小组。LSD1被认为可改变DNA结构和关闭许多基因的表达。
LSD1, which stands for lysine-specific demethylase-1 (and is chemically unrelated to the hallucinogen LSD), regulates the structure of the chromosome by removing a key methylation at histone H3, a core component that warps the DNA into compact conformation. This event triggers the "closure" of DNA structure and shuts down gene expression, such as E-cadherin. Zhou's team showed that the N-terminal portion of Snail molecular functions as a "molecular hook" for recruiting LSD1 to the E-cadherin gene, which, in turn, shuts down the expression of E-cadherin and induces tumor cell invasion and metastasis.
LSD1代表着赖氨酸特异性脱甲基酶-1（化学上与致幻药LSD无关），通过出去组氨酸H3关键的甲基化而调控染色体结构，而后者是将DNA卷曲成致密结构的核心成分。该事件触发了DNA结构的“关闭”和关闭了如E-cadherin基因的表达。周研究小组发现snail分子的N-末端部分可作为“分子钩”将LSD1与E-cadherin基因黏连，这样就可导致E-cadherin表达降低，诱导肿瘤细胞浸润和转移。
"This finding has significant clinical ramification, because chemical compounds or agents that can disrupt the interaction of Snail with LSD1 will have a great therapeutic potential of treating metastatic breast cancer," Zhou said. "Scientists at the Markey Cancer Center are currently exploring this idea and are keen to develop drugs that can treat metastatic cancer."
周说：“这项研究发现具有重要的临床意义，因为能破坏snail与LSD1相互作用的化学物质或药物对转移性乳腺癌的治疗将有重要的治疗价值。Markey癌症中心的科学家们目前正在探讨这个想法，强烈开发能治疗转移性癌的药物。”
Breast cancer is the most common cancer in women. Approximately 90 percent of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells, and the average survival after documentation of metastasis is approximately two years.
乳腺癌是女性最常见的癌症。大约90%乳腺癌死亡是银局部复发和远处转移引起的，乳腺癌转移后平均生存时间大约为2年。
"An understanding of the mechanism underlying the biology of breast cancer metastasis will provide novel therapeutic approaches to combat this life-threatening disease," Zhou said.
周说：“理解乳腺癌转移的机制将为这种威胁生命的疾病提供新的治疗方法。”

2010-05-07 22:14

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每日科学2010年5月4日报道，肯塔基大学Markey癌症中心的科学家们在乳腺癌中发现了一种能使肿瘤细胞向邻近或远处扩散的分子机制，该种过程被称为转移。该发现为针对转移性乳腺癌治疗进行一系列新的研究打开了道路。
由英国分子和细胞生物化学助教教授皮特.周领导的这项研究，主要集中研究肿瘤细胞停止粘附于其他细胞，变为可移动或能扩散到机体的过程。该项研究已论文的形式发表于EMBO杂志上，该杂志是欧洲分子生物学组织的旗舰出版物。
肿瘤细胞在转移开始阶段移动性增加类似于上皮-间质移行（EMT），而EMT是胚胎发育、组织重构和创伤愈合等所必需的。例如，在创伤愈合中，伤口边缘的细胞经历EMT过程并迁移到伤口中间而进行愈合。
在所有EMT过程中，细胞失去称为E-cadherin的细胞-细胞粘附分子的表达，其作为“分子胶水”将细胞互相粘附。乳腺癌细胞为了浸润和转移而可破坏这个过程。当分子胶水被破坏了，肿瘤细胞开始迁移并扩散到机体。
Snail蛋白作为总开关在细胞核内科抑制E-cadherin的表达和诱导EMT发生。以前的研究显示snail在许多类型癌特别是乳腺癌中增高。Snail表达增高与转移、肿瘤细胞生存和肿瘤复发密切相关，因此可预测乳腺癌病人具有较差的临床结局。然而，科学家们还不清楚snail是如何启动E-cadherin下调和诱导乳腺癌转移的。
使用蛋白纯化技术，周和其同事发现了snail与其“罪犯伙伴”，一种称为LSD1的酶相互作用并组成小组。LSD1被认为可改变DNA结构和关闭许多基因的表达。
LSD1代表着赖氨酸特异性脱甲基酶-1（化学上与致幻药LSD无关），通过出去组氨酸H3关键的甲基化而调控染色体结构，而后者是将DNA卷曲成致密结构的核心成分。该事件触发了DNA结构的“关闭”和关闭了如E-cadherin基因的表达。周研究小组发现snail分子的N-末端部分可作为“分子钩”将LSD1与E-cadherin基因黏连，这样就可导致E-cadherin表达降低，诱导肿瘤细胞浸润和转移。
周说：“这项研究发现具有重要的临床意义，因为能破坏snail与LSD1相互作用的化学物质或药物对转移性乳腺癌的治疗将有重要的治疗价值。Markey癌症中心的科学家们目前正在探讨这个想法，强烈开发能治疗转移性癌的药物。”
乳腺癌是女性最常见的癌症。大约90%乳腺癌死亡是银局部复发和远处转移引起的，乳腺癌转移后平均生存时间大约为2年。
周说：“理解乳腺癌转移的机制将为这种威胁生命的疾病提供新的治疗方法。”

2010-05-07 22:15

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