Gain-of-function of mutant p53: mutant p53 enhances cancer progression by inhibiting KLF17 expression in invasive breast carcinoma cells

Ali, Amjad; Shah, Abdus Saboor; Ahmad, Ayaz

doi:10.1016/j.canlet.2014.07.045

Cited by 39 publications

(32 citation statements)

References 33 publications

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“…GSL-II recognizes Nacetyl-D glucosamine on the glycan structure, and this is a source for hyaluronan synthesis and plays a critical role in CD44 (hyaluronan receptor) biology in human cancer [32]. Mutant p53 was recently proved to have gain of function and to be directly bound to KLF17, a tumor suppressor molecule, and augmented CD44 expression by suppressing KLF17 [33]. This intriguing finding may explain our clinical result.…”

Section: Discussionsupporting

confidence: 54%

Lectin microarray technology identifies specific lectins related to lymph node metastasis of advanced gastric cancer

et al. 2015

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Background Although various molecular profiling technologies have the potential to predict specific tumor phenotypes, the comprehensive profiling of lectin-bound glycans in human cancer tissues has not yet been achieved. Methods We examined 242 advanced gastric cancer (AGC) patients without or with lymph node metastasis-N0 (n = 62) or N? (n = 180)-by lectin microarray, and identified the specific lectins highly associated with AGC phenotypes. Results In seven gastric cancer cell lines, in contrast to expressed-in-cancer lectins, not-expressed-in-cancer (NEC) lectins were tentatively designated by lectin microarray. Binding signals of the specific lectins were robustly reduced in AGC patients with N? status as compared with those with N0 status. The receiver operating characteristic curve determined the optimal cutoff value to differentiate N0 status from N? status, and subsequent profiling of NEC lectins identified Vicia villosa agglutinin (VVA) association with the significant other lectins involved in lymph node metastasis. VVA reaction was clearly found on cancer cells, suggesting that it may result from carcinoma-stroma interaction in primary AGC, because VVA is an NEC lectin. Most intriguingly, VVA reaction was remarkably attenuated in the tumor cells of the metastatic lymph nodes, even if it was recognized in primary AGC. In AGC, histological type was strongly associated with soybean agglutinin and Bauhinia purpurea lectin, whereas p53 mutation was the best correlated with Griffonia simplicifolia lectin II. Conclusions Lectin microarrays can be used to very accurately quantify the reaction of glycans with tumor tissues, and such profiles may represent the specific phenotypes, including N? status, histological type, or p53 mutation of AGC.

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Section: Discussionsupporting

confidence: 54%

Lectin microarray technology identifies specific lectins related to lymph node metastasis of advanced gastric cancer

et al. 2015

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“…It is well established that TP53, CDKN2A/p16, and SMAD4/DPC4 mutations occur during pancreatic carcinogenesis, but it is unknown whether these mutations are associated with the abnormal metabolic tumor burden detected by 18 F-FDG PET/CT. Nevertheless, abnormal expression profiles of TP53, CDKN2A/p16, and SMAD4/DPC4 are known to contribute to tumor malignancies and treatment-resistance [23][24][25][26][27]. Activation of transcription factor TP53 in response to a series of stimuli and stresses induces signaling pathways that affect anticancer mechanisms, including DNA repair, cell-cycle arrest and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer

Shi

Qin

et al. 2015

Cancer Letters

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“…Binding to the E2F-4 transcription factor, mutant p53 represses BRCA1 and RAD17 genes impairing the DNA repair mechanism and promoting cancer genomic instability [181]. Mutant p53 is also recruited, together with p300, at the promoter of the proteasome activator REGγ , which promotes p53 wild-type, p21, and p16 protein degradation [182] and inhibits the expression of KLF17 promoting cancer progression in invasive breast cancer cells [183]. Increasing evidence highlight the correlation between mutant p53 and increased cell metabolism associated with cancer progression.…”

Section: P53 and Mutant P53 Protein Functionsmentioning

confidence: 99%

Mutant p53 Protein and the Hippo Transducers YAP and TAZ: A Critical Oncogenic Node in Human Cancers

Ferraiuolo¹,

Blandino²,

Strano³

2017

IJMS

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p53 protein is a well-known tumor suppressor factor that regulates cellular homeostasis. As it has several and key functions exerted, p53 is known as “the guardian of the genome” and either loss of function or gain of function mutations in the TP53 coding protein sequence are involved in cancer onset and progression. The Hippo pathway is a key regulator of developmental and regenerative physiological processes but if deregulated can induce cell transformation and cancer progression. The p53 and Hippo pathways exert a plethora of fine-tuned functions that can apparently be in contrast with each other. In this review, we propose that the p53 status can affect the Hippo pathway function by switching its outputs from tumor suppressor to oncogenic activities. In detail, we discuss: (a) the oncogenic role of the protein complex mutant p53/YAP; (b) TAZ oncogenic activation mediated by mutant p53; (c) the therapeutic potential of targeting mutant p53 to impair YAP and TAZ oncogenic functions in human cancers.

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Gain-of-function of mutant p53: mutant p53 enhances cancer progression by inhibiting KLF17 expression in invasive breast carcinoma cells

Cited by 39 publications

References 33 publications

Lectin microarray technology identifies specific lectins related to lymph node metastasis of advanced gastric cancer

Lectin microarray technology identifies specific lectins related to lymph node metastasis of advanced gastric cancer

Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer

Mutant p53 Protein and the Hippo Transducers YAP and TAZ: A Critical Oncogenic Node in Human Cancers

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