Редактирование: DTL (раздел)

==Publications==

{{medline-entry
|title=Targeting [[DTL]] induces cell cycle arrest and senescence and suppresses cell growth and colony formation through [[TPX2]] inhibition in human hepatocellular carcinoma cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29606879
|abstract=Hepatocellular carcinoma (HCC) has an increasing incidence and high mortality. Surgical operation is not a comprehensive strategy for liver cancer. Moreover, tolerating systemic chemotherapy is difficult for patients with HCC because hepatic function is often impaired due to underlying cirrhosis. Therefore, a comprehensive strategy for cancer treatment should be developed. [[DTL]] (Cdc10-dependent transcript 2) is a critical regulator of cell cycle progression and genomic stability. In our previous study, the upregulation of [[DTL]] expression in aggressive HCC correlated positively with tumor grade and poor patient survival. We hypothesize that targeting [[DTL]] may provide a novel therapeutic strategy for liver cancer. [[DTL]] small interference RNAs were used to knock down [[DTL]] protein expression. A clonogenic assay, immunostaining, double thymidine block, imaging flow cytometry analysis, and a tumor spheroid formation assay were used to analyze the role of [[DTL]] in tumor cell growth, cell cycle progression, micronucleation, ploidy, and tumorigenicity. Our results demonstrated that targeting [[DTL]] reduced cell cycle regulators and chromosome segregation genes, resulting in increased cell micronucleation. [[DTL]] depletion inhibited liver cancer cell growth, increased senescence, and reduced tumorigenesis. [[DTL]] depletion resulted in the disruption of the mitotic proteins cyclin B, [[CDK1]], securin, seprase, Aurora A, and Aurora B as well as the upregulation of the cell cycle arrest gene [i]p21[/i]. A rescue assay indicated that [[DTL]] should be targeted through [[TPX2]] downregulation for cancer cell growth inhibition. Moreover, [[DTL]] silencing inhibited the growth of patient-derived primary cultured HCC cells. Our study results indicate that [[DTL]] is a potential novel target gene for treating liver cancer through liver cancer cell senescence induction. Furthermore, our results provide insights into molecular mechanisms for targeting [[DTL]] in liver cancer cells. The results also indicate several other starting points for future preclinical and clinical studies on liver cancer treatment.

|keywords=* DTL
* TPX2
* cell cycle
* hepatocellular carcinoma
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5868578
}}
{{medline-entry
|title=Expression of aquaporins-1 and -2 during nephrogenesis and in autosomal dominant polycystic kidney disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/8760258
|abstract=Aquaporin-1 ([[AQP1]]), located in proximal tubules (PT) and descending thin limbs of Henle ([[DTL]]), and aquaporin-2 ([[AQP2]]), located in collecting ducts (CD), are channels involved in water transport across renal tubule epithelia. Using antibodies against [[AQP1]] and [[AQP2]], we here show expression of [[AQP1]] and [[AQP2]] in normal human developing and adult kidneys and in autosomal dominant polycystic kidney disease (ADPKD). Unlike in rats, [[AQP1]] and [[AQP2]] are expressed early during human nephrogenesis (12-wk gestation). [[AQP1]] was first seen in developing PT epithelia, predominantly in apical cell membranes, and, at 15 wk, was also detected in [[DTL]]. [[AQP2]] was seen in apical cell membranes of the branching ureteric bud and CD system from 12 wk and throughout development. In adult normal kidneys, [[AQP1]] was localized to apical and basolateral membrane domains of PT and [[DTL]], whereas [[AQP2]] was restricted to principal cells of CD. This distribution of [[AQP1]] and [[AQP2]] was also seen in early stage ADPKD, except that [[AQP1]] was mostly located in the apical membrane region of expanded PT. In end-stage ADPKD, two-thirds of the cysts expressed either [[AQP1]] or [[AQP2]], but these two water channels were never colocalized in the same cyst. Western blot analysis showed maximal expression of [[AQP1]] and [[AQP2]] in normal adult kidneys, lower levels in fetal kidneys, and decreases associated with degree of cystic progression in ADPKD. These data 1) demonstrate specific, mutually exclusive localization of [[AQP1]] and [[AQP2]] in human fetal and adult kidneys; 2) show that both channels are expressed early during nephrogenesis; and 3) show that the mutual exclusivity of localization is maintained even into end-stage ADPKD.
|mesh-terms=* Aging
* Amino Acid Sequence
* Animals
* Animals, Newborn
* Aquaporin 1
* Aquaporin 2
* Aquaporin 6
* Aquaporins
* Blood Group Antigens
* Blotting, Western
* Embryonic and Fetal Development
* Humans
* Immunohistochemistry
* Ion Channels
* Kidney
* Molecular Sequence Data
* Polycystic Kidney, Autosomal Dominant
* Rats
* Reference Values
* Staining and Labeling

|full-text-url=https://sci-hub.do/10.1152/ajprenal.1996.271.1.F169
}}