title: The novel focal adhesion gene kindlin-2 promotes the invasion of gastric             cancer cells mediated by tumor-associated macrophages.
abstract: Kindlin-2 is a novel focal adhesion gene mediating the cell-extracellular             matrix (ECM) adhesion. Tumor-associated macrophages (TAMs) play an important role             in linking chronic inflammation to cancer progression. Both kindlin-2 and TAMs             have been found to promote the invasion of gastric cancer cells in our previous             studies. However, the correlation between kindlin-2 and TAMs remains unclear.             Real-time RT-PCR was used to investigate kindlin-2 expression in the AGS, NCI             and Hs-746T gastric cancer cell lines co-cultured with TAMs under normal or hypoxic             conditions. IL8, IL10, IL11, IL17b, IL18, IL22 and IL24 expressions were measured             by real-time RT-PCR in the gastric cancer lines with varying levels of kindlin-2             expression, as well as after downregulation of kindlin-2 mRNA expression by the             siRNA method. We found that kindlin-2 was upregulated in all three gastric cancer             cell lines when co-cultured with TAMs under normal conditions. Under hypoxic conditions,             the induction of kindlin-2 expression induced by macrophages was significantly             downregulated in the Hs-746T cell line. IL8, IL11, IL17b, IL22 and IL24 expression             was significantly higher in gastric cell lines with high kindlin-2 expression.             Downregulation of kindlin-2 mRNA decreased IL10, IL11, IL17b, IL22 and IL24 expression             but IL8 and IL18 expression was upregulated. Therefore, the novel focal adhesion             gene kindlin-2 may play an important role in promoting the invasion of gastric             cancer cells mediated by TAMs through regulating interleukin expression.
authors.affiliation: Department of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, PR China.
authors.forename: Zhanlong
authors.initials: Z
authors.lastname: Shen
authors.forename: Yingjiang
authors.initials: Y
authors.lastname: Ye
authors.forename: Tuuli
authors.initials: T
authors.lastname: Kauttu
authors.forename: Hanna
authors.initials: H
authors.lastname: Seppänen
authors.forename: Sanna
authors.initials: S
authors.lastname: Vainionpää
authors.forename: Shan
authors.initials: S
authors.lastname: Wang
authors.forename: Harri
authors.initials: H
authors.lastname: Mustonen
authors.forename: Pauli
authors.initials: P
authors.lastname: Puolakkainen
mesh_terms: D002448:Cell Adhesion / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement; D018920:Coculture Techniques; D015536:Down-Regulation / Q000235:genetics; D005109:Extracellular Matrix / Q000502:physiology; D015870:Gene Expression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D007378:Interleukins / Q000235:genetics*; D008264:Macrophages / Q000378:metabolism*; D008565:Membrane Proteins / Q000235:genetics*; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000235:genetics*; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D013274:Stomach Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*
chemical_list: C477322:FERMT3 protein, human; D007378:Interleukins; D008565:Membrane Proteins; D009363:Neoplasm Proteins; D012333:RNA, Messenger