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JNK- and Fos-regulated Mmp1 expression cooperates with Ras to induce invasive tumors in Drosophila.


ABSTRACT: Loss of the epithelial polarity gene scribble in clones of Drosophila imaginal disc cells can cooperate with Ras signaling to induce malignant tumors. Such mutant tissue overproliferates, resists apoptosis, leaves its place of origin and invades other organs, ultimately causing lethality. We show that increased Jun N-terminal kinase (JNK) signaling resulting from the loss of scribble promotes the movement of transformed cells to secondary sites. This effect requires Fos-dependent transcriptional activation of a matrix metalloprotease gene mmp1 downstream of JNK. Expression of the Mmp inhibitor Timp or Mmp RNAi knockdown suppresses cell invasiveness. The proinvasive function of the JNK pathway is revealed in a tumor context when active Ras signaling prevents the apoptotic response to JNK activity as it occurs in nontransformed cells. Based on these results, we present a model that explains the oncogenic cooperation between JNK and Ras, and describes how aberrant regulation of cell survival, proliferation and mobilization cooperate to incite malignant tumor formation.

SUBMITTER: Uhlirova M 

PROVIDER: S-EPMC1636619 | biostudies-literature | 2006 Nov

REPOSITORIES: biostudies-literature

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Lacrimal Sac Sebaceous Carcinoma.

Vahdani Kaveh K   Coupland Sarah E SE   Ashdown Morag Evalyn ME   Garrott Hellen H   Ford Rebecca R  

Ophthalmic plastic and reconstructive surgery 20190701 4


Sebaceous carcinoma is an aggressive malignancy with a high mortality rate that commonly arises in the periorbital area. Rarely, the lacrimal apparatus may be involved by either contiguous or noncontiguous spread. The authors describe 2 unusual cases of sebaceous carcinoma in the lacrimal sac, presenting as a medial canthal mass simulating chronic dacryocystitis. In Case 1, the sebaceous carcinoma occurred primarily in the lacrimal sac, in the absence of concurrent or previous ocular adnexal seb  ...[more]

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