Рак молочной железы “базального” фенотипа, в отличие от “люменального”, более агрессивен и плохо лечится. Показано, что важнейшую роль в регуляции механизмов транскрипции, поддерживающих “базальный” фенотип рака молочной железы, играет сумоилирование белка TFAP2А. Подавление сумоилирования может стать эффективной стратегией лечения базального рака.

Рак молочной железы – самое распространенное онкологическое заболевание женщин. Созданная в последнее время клиническая классификация его подтипов по профилю экспрессирующихся генов позволяет предсказывать исход заболевания и определять рациональную терапию. Но о механизмах регуляции транскрипции, определяющих эти подтипы, известно еще очень мало. Было известно, что функция TFAP2C - одного из генов семейства АР-2, чрезвычайно важна для поддержания люменального фенотипа рака, для индукции генов, свойственных этому фенотипу, и для репрессии генов, свойственных другому, более агрессивному базальному фенотипу. Несмотря на очень сильное сходство с TFAP2C, функции другого гена семейства TFAP2А сильно отличались. С целью получить важные данные для разработки стратегии создания противораковых средств авторы изучили функциональные различия белков TFAP2C и TFAP2А в регуляции “люменальных” генов.

В экспериментах на культурах клеток на уровне как мРНК, так и белков было показано, что выключение TFAP2C подавляет экспрессию “люменальных” генов, а выключение TFAP2А на нее практически не влияет. Активный ген TFAP2С подавлял экспрессию “базальных” генов, а TFAP2А на нее не действовал. В то же время анализ участков генома, с которыми связывались продукты этих двух генов показал их практическую идентичность. Следовательно, функциональные различия TFAP2C и TFAP2А не связаны с их взаимодействием с регуляторными областями генов-мишеней.

Эксперименты с гибридными белками, в которых отдельные участки TFAP2А замещались гомологичными участками TFAP2С показали, что область TFAP2С, ответственная за “люменальную” активацию, расположена в пределах первых 128 аминокислотных остатков. Блок активности TFAP2А на “люменальных” промоторах мог быть связан как с дополнительными коактиваторами, специфичными лишь для TFAP2С, так и с промотор-специфическими репрессорами TFAP2А. Проверка множества факторов, взаимодействующих с TFAP2C и TFAP2А показала, что активация TFAP2А на “люменальных” промоторах может быть достигнута путем инактивации двух генов, контролирующих путь присоединения к нему белков SUMO (small ubiquitin-like modifier). Замена K10R в TFAP2А также резко понижала уровень его сумоилирования и придавала способность активировать “люменальные” гены.

Выключение TFAP2C в культивируемых клетках придавало им “базальный” фенотип. Если же в них вводили TFAP2А-K10R, но не TFAP2А дикого типа, “люменальный” фенотип восстанавливался. Аналогичный эффект давало подавление сумоилирования специфическим ингибитором.

Обработка культур клеток базального рака ингибиторами сумоилирования перед введением их мышам подавляла образование опухолей. Более того, введение необработанных клеток на фоне “терапии” ингибиторами дало аналогичный результат. Токсического эффекта ингибиторов при этом не наблюдалось.

Таким образом показано, что сумоилирование играет важнейшую роль в регуляции механизмов транскрипции, поддерживающих “базальный” фенотип рака молочной железы. Подавление сумоилирования может стать эффективной стратегией лечения базального рака.
авторский текст

Рисунок: Сумоилирование белка TFAP2A требуется для поддержания высокоагрессивного базального фенотипа рака молочной железы. Блок сумоилирования придает опухоли менее агрессивный люменальный фенотип.

Источник: Bogachek MV, Chen Y, Kulak MV, Woodfield GW, Cyr AR, Park JM, Spanheimer PM, Li Y, Li T, Weigel RJ. Sumoylation pathway is required to maintain the basal breast cancer subtype. // Cancer Cell. 2014; V. 25: P. 748-761.

Рак это ужасно...

Обработка культур клеток базального рака ингибиторами сумоилирования перед введением их мышам подавляла образование опухолей.
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