Molecular background of the regional lymph node metastasis of gastric cancer (Review)

Abstract

Abstract. Gastric cancer (GC) is one of the deadliest types of cancer in the world. Lymph node (LN) metastasis is a complex and malignant behavior of GC, involving a sequence of biological processes, including decreased adherence to adjacent cells, extracellular matrix (ECM) degradation and lymphatic channel permeation. LN metastasis is directly associated with the treatment response, local recurrence and long-term survival of patients with GC. Therefore, the molecular mechanisms of LN metastasis in GC development require further investigation. Recently, a large number of clinical studies have focused on the molecular mechanisms and biological markers of tumor invasion and metastasis. However, few articles have broadly summarized LN metastasis in GC, and the molecular mechanisms of LN metastasis are not yet fully understood. In the present review, the molecular mechanisms of LN metastasis in GC will be discussed, including the following aspects: Cell adhesion and movement, ECM degradation, new vessel formation, and molecular pattern differences between metastatic LNs and the primary tumor. This review may lead to a better understanding of LN metastasis in GC, and the identification of new diagnostic markers.

Resveratrol suppresses the growth and metastatic potential of cervical cancer by inhibiting STAT3Tyr705 phosphorylation

“…Metastasis is a complicated biological process that involves primary tumor angiogenesis, cancer cell invasion, vascular intravasation, distant target organ extravasation, and colonization of a foreign microenvironment by invading cells. Primary epithelial cancer cells can acquire migration and invasion abilities [46][47][48] with EMT. Matrix metalloproteinases (MMPs) degrade ECM around invasive cancer cells and facilitate vascular intravasation of cancer cells.…”

Evaluation of the correlation of vasculogenic mimicry, Notch4, DLL4, and KAI1/CD82 in the prediction of metastasis and prognosis in non-small cell lung cancer

“…There is increasing evidence that cell surface adhesion proteins and ECM components are critical for tumor metastasis. [42,43] KAI1/CD82 is cell membrane protein that bind to ECM or adhesion protein. [24,44] Moreover, KAI1/CD82 can prevent angiogenesis by inhibiting the epithelial-mesenchymal transition (EMT), and further inhibit tumor invasion and metastasis.…”

Overexpressed MAGP1 Is Associated With a Poor Prognosis and Promotes Cell Migration and Invasion in Gastric Cancer

“…And Fibrillin-1 can indirectly mediate TGF-β pathway by binding MAGP1, which tethered the active form of TGF-β to the microfibril (30). Meanwhile, ECM was reported to play an important role in metastasis of GC (31). The interaction between MAGP1 and ECM indicates MAGP1 may contribute to migration and invasion of GC cells.…”