Expression of PTEN and Its Correlation with Proliferation Marker                     Ki-67 in Head and Neck Cancer

Ahmed, Malik Waqar; Kayani, Mahmood Akhtar; Shabbir, Ghulam; Ali, Shariq; Shinwari, Wajih-ud-din; Mahjabeen, Ishrat

doi:10.5301/jbm.5000196

Cited by 19 publications

(9 citation statements)

References 76 publications

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“…Some researches revealed the significant association between no/low PTEN expression and T stage, N stage and/or grade [58,62]. However, there are studies where such relations were not found [61,63], similarly to us. On the other hand, in our study expression of PTEN was significantly associated with cancer site.…”

Section: Pten and Pptensupporting

confidence: 67%

EGFR/PI3K/Akt/mTOR pathway in head and neck squamous cell carcinoma patients with different HPV status

Janecka-Widła¹,

Majchrzyk²,

Mucha-Małecka³

et al. 2021

pjp

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The aim of the study was to compare prognostic potential of PIK3CA mutations and expression of proteins involved in or regulate EGFR/PI3K/Akt/mTOR signaling in HPV16 positive and HPV negative head and neck squamous cell carcinoma (HNSCC) patients. The expression of proteins (EGFR, Akt, pAkt(Ser473), pAkt(Thr308), mTOR, PTEN, pPTEN, APOBEC3B) were assessed immunohistochemically and PIK3CA mutations (p.E542K, p.E545K, p.H1047R) by qPCR. Significantly more HPV16 positive tumors (89.29%) with low EGFR expression were found as compared to HPV negative ones (58.82%). PIK3CA mutations were detected in 7.14% of HPV16 positive and 2.5% of HPV negative cancers. In HPV16 positive patients survival analysis has shown that positive prognostic potential for disease free survival (DFS) had low expression of APOBEC3B. In HPV negative patients prognostic significance for DFS had APOBEC3B, Akt and pAkt(Thr308) levels, and for overall survival (OS) -pAkt(Thr308) only. Independent favorable prognostic factors in the whole group of patients were: low T stage, low pAkt(Thr308) expression, active HPV16 infection (for OS and DFS) and female gender (for OS). Obtained results suggest the existence of significant differences in expression and prognostic potential of proteins involved in EGFR/PI3K/Akt/mTOR signaling between HPV16 positive and HPV negative HNSCC patients.

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Section: Pten and Pptensupporting

confidence: 67%

EGFR/PI3K/Akt/mTOR pathway in head and neck squamous cell carcinoma patients with different HPV status

Janecka-Widła¹,

Majchrzyk²,

Mucha-Małecka³

et al. 2021

pjp

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“…The PI3K/AKT signaling pathway is a well-known pathway in the regulation of tumorigenesis, and is significantly activated in glioma [ 14 ]. PTEN contributes in antagonizing PI3K [ 15 ], thereby weakening AKT activation [ 16 ], which could suppress down-stream products thereby inducing cell cycle arrest in the G1 phase by increasing ki-67 expression [ 15 ] and decreasing cyclin D1 expression [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway

Liu

et al. 2017

J Neurooncol

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Spalt-like transcription factor 4 (SALL4), a oncogene, is known to participate in multiple carcinomas, and is up-regulated in glioma. However, its actual role and underlying mechanisms in the development of glioma remain unclear. The present study explored the molecular functions of SALL4 in promoting cell proliferation in glioma. The expression level of SALL4 in 69 human glioma samples and six non-tumor brain tissues was determined using real-time polymerase chain reaction (PCR). Then, we transfected U87 and U251 cell lines with siRNA, and assessed cellular proliferation and cell cycle to understand the function of SALL4, and the relationship between SALL4, PTEN and PI3K/AKT pathway. PCR confirmed that the expression of SALL4 was higher in the glioma samples than non-tumor brain tissues. Cellular growth and proliferation were dramatically reduced following inhibition of SALL4 expression. Western blot showed increase in PTEN expression when SALL4 was silenced, which in turn depressed the activation of PI3K/AKT pathway, suggesting that PTEN was a downstream target of SALL4 in glioma development. Therefore, SALL4 could act as a proto-oncogene by regulating the PTEN/PI3K/AKT signaling pathway, thereby facilitating proliferation of glioma cells.

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“…In addition, we found that the expression of PTEN was dramatically up-regulated. PTEN is an important negative regulator of AKT pathway, it can antagonize PI3K and then weaken the activation of AKT (Zhang et al, 2015 ; Ahmed et al, 2016 ). Therefore, the up-regulation of PTEN and down-regulation of PI3K further confirmed that AKT pathway could be inactivated by CT04.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of RhoA-Subfamily GTPases Suppresses Schwann Cell Proliferation Through Regulating AKT Pathway Rather Than ROCK Pathway

Tan

Wen

et al. 2018

Front. Cell. Neurosci.

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Inhibiting RhoA-subfamily GTPases by C3 transferase is widely recognized as a prospective strategy to enhance axonal regeneration. When C3 transferase is administered for treating the injured peripheral nerves, Schwann cells (SCs, important glial cells in peripheral nerve) are inevitably impacted and therefore SC bioeffects on nerve regeneration might be influenced. However, the potential role of C3 transferase on SCs remains elusive. Assessed by cell counting, EdU and water-soluble tetrazolium salt-1 (WST-1) assays as well as western blotting with PCNA antibody, herein we first found that CT04 (a cell permeable C3 transferase) treatment could significantly suppress SC proliferation. Unexpectedly, using Y27632 to inhibit ROCK (the well-accepted downstream signal molecule of RhoA subfamily) did not impact SC proliferation. Further studies indicated that CT04 could inactivate AKT pathway by altering the expression levels of phosphorylated AKT (p-AKT), PI3K and PTEN, while activating AKT pathway by IGF-1 or SC79 could reverse the inhibitory effect of CT04 on SC proliferation. Based on present data, we concluded that inhibition of RhoA-subfamily GTPases could suppress SC proliferation, and this effect is independent of conventional ROCK pathway but involves inactivation of AKT pathway.

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Expression of PTEN and Its Correlation with Proliferation Marker Ki-67 in Head and Neck Cancer

Abstract: Our data suggest that downregulation of PTEN and overexpression of Ki-67 may contribute to the initiation and progression of HNC.

Cited by 19 publications

References 76 publications

EGFR/PI3K/Akt/mTOR pathway in head and neck squamous cell carcinoma patients with different HPV status

EGFR/PI3K/Akt/mTOR pathway in head and neck squamous cell carcinoma patients with different HPV status

SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway

Inhibition of RhoA-Subfamily GTPases Suppresses Schwann Cell Proliferation Through Regulating AKT Pathway Rather Than ROCK Pathway

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