HSPD1 repressed E-cadherin expression to promote cell invasion and migration for poor prognosis in oral squamous cell carcinoma

Abstract

Buccal mucosa squamous cell carcinoma (BMSCC) is one of major subsites of oral cancer and is associated with a high rate of metastasis and poor prognosis. Heat shock proteins (HSPs) act as potential prognostic biomarkers in many cancer types. However, the role of HSPD1 in oral cancer, especially in BMSCC, is still unknown. Through data analysis with The Cancer Genome Atlas (TCGA), we found the association of HSPD1 gene expression with tumorigenesis and poor prognosis in oral cancer patients. Our cohort study showed that higher HSPD1 protein level was associated with tumorigenesis and poor prognosis in BMSCC patients with lymph node invasion, suggesting that HSPD1 may be involved in tumor metastasis. Moreover, knockdown of HSPD1 induced E-cadherin expression and decreased the migration and invasion of BMSCC cells. In contrast, ectopic expression of HSPD1 diminished E-cadherin expression and promoted the migration/invasion of BMSCC cells. Further, HSPD1 regulated RelA activation to repress E-cadherin expression, enhancing the migration and invasion of BMSCC cells. Furthermore, HSPD1 protein level was inversely correlated with E-cadherin protein level in tumor tissues and co-expression of high HSPD1/low E-cadherin showed a significant association with poor prognosis in BMSCC patients. Taken together, HSPD1 might repress E-cadherin expression and promote metastatic characters of BMSCC cells for poor prognosis of BMSCC patients.

<p>Genipin Induces Autophagy and Suppresses Cell Growth of Oral Squamous Cell Carcinoma via PI3K/AKT/MTOR Pathway</p>

“…At present, OSCC remains a major threat to increased morbidity and poor 5-year survival. 2 Although OSCC has advantages of timely treatment due to relatively easier access for early diagnosis, it is also an aggressive disease with local recurrence and cervical lymph node metastasis. 2 The basic method of therapy includes surgical resection leaving a margin of healthy tissue, and neck dissection during node metastases.…”

“…2 Although OSCC has advantages of timely treatment due to relatively easier access for early diagnosis, it is also an aggressive disease with local recurrence and cervical lymph node metastasis. 2 The basic method of therapy includes surgical resection leaving a margin of healthy tissue, and neck dissection during node metastases. 20,21 However, conventional therapy often leads to impaired oral functions.…”

“…Oral cancer is an increasing threat worldwide, with around 640,000 new cases being detected annually globally. 1,2 In addition, there are 145,000 deaths per year in oral cancer, 3 and five-year survival rates of patients with advanced oral cancer are 30-40%. 4 Owing to the lack of early symptoms and appropriate screening for precancerous lesions, most oral cancer cases are not detected until later stages.…”

Human Papillomavirus 16 E7 Promotes EGFR/PI3K/AKT1/NRF2 Signaling Pathway Contributing to PIR/NF-κB Activation in Oral Cancer Cells

“…Prominent activators of NF-κB signaling are tumor necrosis factor receptor (TNFR) family members, lipopolysaccharides (LPS) and EGFR [ 40 , 41 ], in fact, EGFR and NF-κB are described as co-directional activation signaling pathways in some carcinomas, such as HNCs [ 42 ]. Once activated, NF-κB regulates the expression of genes involved in different cellular events, including EMT and cancer progression, a process that is strongly related to E-cadherin downregulation and N-cadherin upregulation [ 43 , 44 , 45 ]. Pirin is relevant during NF-κB signaling, working as transcriptional factor with Rel-A protein (p65) [ 46 ] and, importantly, Pirin has also been described as an EMT regulator by decreasing E-cadherin expression [ 22 , 47 ].…”

The expression profiles and prognostic values of HSPs family members in Head and neck cancer

“…It has been described as a potential prognostic and diagnostic biomarker for cancer. Recent studies have demonstrated that HSPD1 not only regulates the stability of survivin protein, but also regulates the mRNA expression of survivin [10]. SER-PINH1, also called heat shock protein 47 (HSP47), is a collagen specific molecular chaperone.…”