Underlying Facets of Cancer Metastasis

Tyagi, Abhishek

doi:10.3390/cancers14122989

Cited by 1 publication

(1 citation statement)

References 10 publications

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“…Malignant tumors induce lymphatic dilation (lymphangiogenesis) in the primary tumor and the drainage sentinel area by releasing lymphatic growth factors such as VEGF-C and LYVE1, thereby promoting LN metastasis [ 58–61 ]. Moreover, EMT is known to drive the metastasis of cervical cancer cells to LNs [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

CEACAM5 inhibits the lymphatic metastasis of head and neck squamous cell carcinoma by regulating epithelial–mesenchymal transition via inhibiting MDM2

Wang

Pan

et al. 2022

Clinical Science

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Lymph node (LN) metastasis affects both the management and prognosis of head and neck squamous cell carcinoma (HNSCC). Here, we explored the relationship between lymphatic metastasis and CEA family member 5 (CEACAM5), including its possible regulatory role in HNSCC. The levels of CEACAM5 in tissues from patients with HNSCC, with and without LN metastases, were assessed by transcriptome sequencing. The associations between CEACAM5 and the N stage of LN metastasis in HNSCC were predicted through The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases and a pan-cancer analysis of CEACAM5 expression in 33 common human tumors was conducted. CEACAM5 levels were analyzed in tumor and normal tissue specimens from HNSCC patients and the correlation between CEACAM5 levels and prognosis was evaluated. The influence of CEACAM5 on cell proliferation, invasion, migration, and apoptosis was investigated in HNSCC cell lines, as were the downstream regulatory mechanisms. A mouse model of LN metastasis was constructed. CEACAM5 levels were significantly higher in HNSCC tissue without LN metastasis than in that with LN metastasis. Similar findings were obtained for the clinical specimens. CEACAM5 levels were associated with better clinical prognosis. CEACAM5 was found to inhibit the proliferation and migration and promote the apoptosis of HNSCC cells. A mouse xenograft model showed that CEACAM5 inhibited LN metastasis. In conclusions, CEACAM5 inhibited epithelial–mesenchymal transition in HNSCC by reducing murine double minute 2 (MDM2) expression and thereby suppressing LN metastasis. CEACAM5 has potential as both a prognostic marker and a therapeutic target in HNSCC.

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Section: Discussionmentioning

confidence: 99%