TIMP3, DAPK1 and AKR1B10 are important for squamous cell lung cancer tumorogenesis while AKR1B10 is potential oncogene whereas TIMP3 and DAPK1 are potential tumor suppressor genes.

TIMP3 overexpression correlates with progression of non-small cell lung cancer.

The expression of TIMP-3 in the non-small cell lung cancer and metastasis groups was downregulated.

we show that KDM1A promotes cancer metastasis in non-small cell lung cancer cells by repressing TIMP3 (tissue inhibitor of metalloproteinase 3) expression.

IL-32gamma may increase TIMP-3 expression via hypomethylation through inactivation of NF-kappaB activity, and thereby reduce lung tumor growth.

ALKBH5 repressed TIMP3 mRNA stability and protein production. In conclusion, the present research confirmed the ALKBH5/TIMP3 pathway in the non small lung cancer (NSCLC) oncogenesis progress, providing a novel insight for the epitranscriptome and potential therapeutic target for NSCLC.

Associations of TIMP-3 Genetic Polymorphisms with EGFR Statuses and cancer Clinicopathologic Development in lung Adenocarcinoma Patients.

TIMP-3 regulates MMP-2 activation to limit tumor cell extravasation and subsequent colonization of the lung, without augmenting inflammatory cell response.