Promoter hypermethylation-mediated down-regulation of LATS1 and LATS2 in human astrocytoma

  title={Promoter hypermethylation-mediated down-regulation of LATS1 and LATS2 in human astrocytoma},
  author={Zheng Jiang and Xingang Li and Jin Hu and Wei Zhou and Da-ru Lu},
  journal={Neuroscience Research},

Molecular Alterations and Expression Dynamics of LATS1 and LATS2 Genes in Non-Small-Cell Lung Carcinoma

LATS1 is an independent prognostic factor and may play an important role inNSCLC progression and may serve as a novel therapeutic target of NSCLC.

Decreased expression of LATS1 is correlated with the progression and prognosis of glioma

It is found that mRNA and protein of LATS1 expression is significantly downregulated in glioma compared with normal control brain tissues and its downregulated expression may contribute toglioma progression.

LATS2 is De-methylated and Overexpressed in Nasopharyngeal Carcinoma and Predicts Poor Prognosis

Functional studies showed that the suppression of LATS2 expression in nasopharyngeal carcinoma (5-8F and CNE2) cell lines by using specific small interfering (siRNA) resulted in the inhibition of growth, induction of apoptosis and S-phase cell cycle increase.

Alterations in the NF2/LATS1/LATS2/YAP Pathway in Schwannomas

The results suggest that an abnormal Hippo signaling pathway is involved in the pathogenesis of most sporadic schwannomas.

Methylation‑associated inactivation of LATS1 and its effect on demethylation or overexpression on YAP and cell biological function in human renal cell carcinoma.

For the first time, the inactivation of LATS1 by promoter methy-lation is demonstrated and it is a tumor suppressor in kidney cancer.

Expression of LATS1 contributes to good prognosis and can negatively regulate YAP oncoprotein in non-small-cell lung cancer

The results indicate that LATS1 may play an important role in NSCLC, and may serve as a novel therapeutic target of NSCLE, and could regulate the nuclear location of YAP.

Underexpression of LATS1 TSG in colorectal cancer is associated with promoter hypermethylation.

Investigating large tumor suppressor 1 (LATS1) expression, promoter hypermethylation, and microsatellite instability in colorectal cancer (CRC) found reduced expression may promote progression of CRC.

Hypermethylation of promoter region of LATS1--a CDK interacting protein in oral squamous cell carcinomas--a pilot study in India.

This is the first study to have explored and identified positive association between LATS1 promoter hypermethylation with histopathological features in oral squamous cell carcinomas.

Kpm/Lats2 is linked to chemosensitivity of leukemic cells through the stabilization of p73.

The results suggest that Kpm/Lats2 is involved in the fate of p73 through the phosphorylation of YAP2 by Kpm or Lats2 and the induction of p 73 target genes that underlie chemosensitivity of leukemic cells.



Down-Regulation of LATS1 and LATS2 mRNA Expression by Promoter Hypermethylation and Its Association with Biologically Aggressive Phenotype in Human Breast Cancers

Hypermethylation of the promoter regions of LATS1 and LATS2 likely plays an important role in the down-regulation of their mRNA levels in breast cancers, and breast cancers with a decreased expression of Lats2 mRNA levels have a biologically aggressive phenotype.

Lats2, a putative tumor suppressor, inhibits G1/S transition

A model in which a combination of mammalian Lats2 and Lats1 control cell proliferation by negatively regulating different cell cycle check points is proposed.

Hypermethylation, but not LOH, is associated with the low expression of MT1G and CRABP1 in papillary thyroid carcinoma

LOH is a remarkably rare mechanism of loss of gene function in PTC and MT1G and CRABP1 are novel genes that are likely involved in the pathogenesis of sporadic PTC.

Promoter hypermethylation of cancer-related genes: a strong independent prognostic factor in acute lymphoblastic leukemia.

The methylation profile may be a potential new biomarker of risk prediction in ALL and was an independent prognostic factor in predicting DFS and OS at 11 years.

Molecular Alterations of h-warts/LATS1 Tumor Suppressor in Human Soft Tissue Sarcoma

The data suggest that the molecular alterations of the h-warts/LATS1 could be of pathologic importance in human sarcomagenesis.

Demethylation of a hypermethylated P15/INK4B gene in patients with myelodysplastic syndrome by 5-Aza-2'-deoxycytidine (decitabine) treatment.

The emergence of partially demethylated epigenotypes and re-establishment of normal p15 protein expression following the initial decitabine courses implicate pharmacologic demethylation as a possible mechanism resulting in hematologic response in MDS.

LATS1 tumor suppressor regulates G2/M transition and apoptosis

The results indicate that the Lats1 tumor suppressor may play an important role in the control of human tumor development and that LATS1 suppresses tumorigenesis by negatively regulating cell proliferation and modulating cell survival.

Methylation profiles of thirty four promoter-CpG islands and concordant methylation behaviours of sixteen genes that may contribute to carcinogenesis of astrocytoma

The established concordant methylation profiles of the subsets consisting of two to three target genes may provide useful clues to the development of the useful prognostic as well as diagnostic assays for astrocytoma.

A gene hypermethylation profile of human cancer.

An unusual view of the pervasiveness of DNA alterations, in this case an epigenetic change, in human cancer is provided and a powerful set of markers are provided to outline the disruption of critical pathways in tumorigenesis and for derivation of sensitive molecular detection strategies for virtually every human tumor type.

Upregulation of BNIP3 by 5-aza-2′-deoxycytidine sensitizes pancreatic cancer cells to hypoxia-mediated cell death

BNIP3 expression is silenced in some pancreatic cancer cells by the methylation of its CpG island, and Demethylation of BNIP3, using a methyltransferase inhibitor, restores the gene’s expression and induces hypoxia-mediated cell death.