Elective neck dissection versus observation for early-stage oral squamous cell carcinoma: Systematic review and meta-analysis

Oh, Lawrence; Phan, Kevin; Kim, S.W.; Low, Tsu-Hui Hubert; Gupta, Ruta; Clark, Jonathan

doi:10.1016/j.oraloncology.2020.104661

Cited by 42 publications

(27 citation statements)

References 41 publications

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“…Recently, Chu et al proved that Taiwanese men exposed to higher concentrations of PM2.5 have an increased risk of oral cancer 2 . The seventh most common cancer in the world is OSCC which has been considered to cause detriment to human health and high mortality 24 . Surfactin is a bacterial cyclic lipopeptide generated by Bacillus subtilis 15 .…”

Section: Discussionmentioning

confidence: 99%

Surfactin from Bacillus subtilis induces apoptosis in human oral squamous cell carcinoma through ROS-regulated mitochondrial pathway

Vo¹,

Liu²,

Wu³

et al. 2020

J. Cancer

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Recently, ambient air particulate matter (PM) has been shown to increase the risk of oral cancer. The most common malignant tumor in the oral cavity is oral squamous cell carcinoma (OSCC). Recent studies have revealed that surfactin, a cyclic lipopeptide generated by Bacillus subtilis , has anti-inflammatory and anti-cancer properties. However, the exact anti-cancer effects of surfactin on human OSCC and underlying molecular mechanisms remain largely unknown. In the present study, we found that treatment of SCC4 and SCC25 cells (human OSCC cell lines) with surfactin reduced the viability of SCC4 and SCC25 cells by induction of apoptosis. Surfactin-induced apoptosis was associated with caspase activation and poly(ADP-ribose) polymerase (PARP) cleavage and was regulated by the mitochondrial pathway, exemplified by mitochondrial depolarization, mitochondrial-derived reactive oxidative species (ROS) production, cytochrome c release, up-regulation of Bad and Bax, and down-regulation of Bcl-2. Surfactin induced NADPH oxidase-dependent ROS generation, which appeared essential for the activation of the mitochondrial pathway. Surfactin-induced mitochondrial-derived ROS generation was associated with JNK1/2 activation. After treatment with surfactin, ROS caused JNK1/2-dependent cell death of SCC4 and SCC25 cells. Taken together, our findings suggest that surfactin induces mitochondria associated apoptosis of human OSCC cell lines, and surfactin may be a potential chemotherapeutic agent for future OSCC treatment.

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Section: Discussionmentioning

confidence: 99%

Surfactin from Bacillus subtilis induces apoptosis in human oral squamous cell carcinoma through ROS-regulated mitochondrial pathway

Vo¹,

Liu²,

Wu³

et al. 2020

J. Cancer

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show abstract

“…Chu et al proved that Taiwanese men exposed to higher concentrations of PM2.5 have an increased risk of oral cancer [2]. The seventh most common cancer in the world is OSCC [27]. A very important step in tumor metastasis is that cancer cells invade the surrounding tissues and vasculature.…”

Section: Discussionmentioning

confidence: 99%

Surfactin from Bacillus subtilis attenuates ambient air particulate matter-promoted human oral cancer cells metastatic potential

Lee

et al. 2020

J. Cancer

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Recently, many studies have indicated that ambient air particulate matter (PM) can increase the risk of oral cancer. The most common malignant tumor in the oral cavity is oral squamous cell carcinoma (OSCC). Usually, cancer cell migration/invasion is the most important cause of cancer mortality. Matrix metalloproteinase-2 (MMP-2) and MMP-9 have been shown to play important roles in regulating metastasis and the tumor microenvironment. Here, we studied the anti-cancer effects of surfactin, a cyclic lipopeptide generated by Bacillus subtilis, on cancer cell migration and invasion. Surfactin suppressed PM-promoted cell migration and invasion and colony formation of SCC4 and SCC25 human oral squamous cell carcinoma cell lines. We observed that PM induced MMP-2 and MMP-9 expression, which was inhibited by surfactin. Transfection with p65, p50, c-Jun, c-Fos, p85, p110, Akt, mammalian target of rapamycin (mTOR), or interleukin-6 (IL-6) siRNA markedly inhibited PM-induced MMP-2 and MMP-9 expression. Moreover, surfactin could reduce Akt, mTOR, p65, and c-Jun activation and IL-6 secretion induced by PM. Finally, we proved that transfection with Akt, p65, or c-Jun siRNA significantly inhibited PM-induced IL-6 release. Taken together, these results suggest that surfactin functions as a suppressor of PM-induced MMP2/9-dependent oral cancer cell migration and invasion by inhibiting the activation of phosphoinositide 3-kinase (PI3K)/Akt/mTOR and PI3K/Akt/nuclear factor-κB (NF-κB) and activator protein-1 (AP-1)/IL-6 signaling pathways.

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“…Some investigators advocate for END only in T2 and higher lesions of the oral cavity, and recommend SNB in small T1 lesions with an N0 neck [135][136][137]. A meta-analysis by Oh et al showed a statistically significant difference in recurrence rate, overall as well as disease-specific survival in the END group at any stage, and this result has been echoed in other similar studies, regardless of the oral cavity subsite [138][139][140]. Moreover, Fasunla et al [141] performed a meta-analysis of 4 randomized control trials (RCT) including 283 patients created another robust argument in favour of END in the clinically node-negative neck.…”

Section: Surgical Therapymentioning

confidence: 99%

The N0 Neck in Oral Squamous Cell Carcinoma A Comprehensive Review and Update on Diagnosis and Management

Patel¹

2020

GJO

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Oral cavity cancer represents one of the most devastating diseases worldwide, as the morbidity and mortality associated with it can be quite significant. Spread to cervical lymph nodes represents a major contributor to patient prognosis, however, despite many technological advances, accurate and consistent identification of involvement of the neck in early stage oral squamous cell carcinoma remains a major challenge. With increasingly sensitive and specific imaging modalities, cytological analysis, as well as sentinel node biopsy, identification of regional cervical metastasis continuously improves. The spread of this disease to regional lymph nodes of the neck often results in dramatic changes in treatment and prognosis, and thus management of the neck in early oral cancer is of paramount importance. A consensus on the ideal treatment modality for the clinically node-negative neck still eludes us, with elective neck dissection at the time of primary treatment being the current gold standard, with radiation and chemotherapy having adjunctive roles. The "wait and see" philosophy also has its advocates, as well as its critics. Advances in genetic analysis of tumours may represent the future in patient-specific intervention. This article represents a review of past, present, as well as future advances in the diagnosis and management of the N0 neck in oral cancer, highlighting the most recent research, techniques, and practices worldwide.

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Elective neck dissection versus observation for early-stage oral squamous cell carcinoma: Systematic review and meta-analysis

Cited by 42 publications

References 41 publications

Surfactin from Bacillus subtilis induces apoptosis in human oral squamous cell carcinoma through ROS-regulated mitochondrial pathway

Surfactin from Bacillus subtilis induces apoptosis in human oral squamous cell carcinoma through ROS-regulated mitochondrial pathway

Surfactin from Bacillus subtilis attenuates ambient air particulate matter-promoted human oral cancer cells metastatic potential

The N0 Neck in Oral Squamous Cell Carcinoma A Comprehensive Review and Update on Diagnosis and Management

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