Publications by authors named "Mashael S Al-Mutairi"

Objectives: Nuclear factor κB (NF-κB) is a superfamily of transcription factors that plays a key role in cancer genesis and progression. The present study aimed to examine the expression of NF-κB/p65 in breast cancer and its relationship with prognostic markers such as tumour grade, tumour size, hormone receptors, and HER-2.

Methods: Ninety-nine unselected formalin-fixed paraffin-embedded invasive ductal and lobular tissue sections were evaluated by immunohistochemistry methods to measure the expression of NF-κB/p65, oestrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor-2 (HER-2), and Ki-67.

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Article Synopsis
  • * The study investigates the role of DUSP4/MKP-2, a regulator of the JNK pathway, in Dox-induced EMT in breast cancer cells, finding that high MKP-2 levels are common in breast cancer tissues.
  • * Results indicate that silencing MKP-2 enhances Dox sensitivity by activating the JNK pathway, leading to reduced EMT and increased cell death, suggesting MKP-2 as a potential target for overcoming Dox resistance in breast cancer.
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Background: Camel urine (CU) has been used as traditional treatment in the Arabian Peninsula for centuries. Although, researchers have reported CU anti-cancer effects, the exact mechanism(s) of action involved has not been fully elucidated. The epithelial-mesenchymal transition EMT is a phenotypic switch that promotes the acquisition of a fibroblastoid-like morphology by epithelial tumor cells, resulting in enhanced tumor cell motility and invasiveness.

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In this study we generated a novel dual specific phosphatase 4 (DUSP4) deletion mouse using a targeted deletion strategy in order to examine the role of MAP kinase phosphatase-2 (MKP-2) in immune responses. Lipopolysaccharide (LPS) induced a rapid, time and concentration-dependent increase in MKP-2 protein expression in bone marrow-derived macrophages from MKP-2(+/+) but not from MKP-2(-/-) mice. LPS-induced JNK and p38 MAP kinase phosphorylation was significantly increased and prolonged in MKP-2(-/-) macrophages whilst ERK phosphorylation was unaffected.

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