Our previous study demonstrated that programmed cell death protein 4 (PDCD4), which is a tumour suppressor gene, is a target of microRNA‑21 (miR‑21), which affects the proliferation and transformation capabilities of renal cell carcinoma (RCC) cells.
Programmed cell death 4 (PDCD4) has been identified as a tumor‑suppressor gene that inhibits neoplastic transformation, tumor progression, and protein translation.
In this review, we focus on the suppression mechanisms of PDCD4 protein that is induced by the tumor promotors EGF and TPA, and in the inflammatory conditions.
Programmed cell death factor 4 (PDCD4) has previously been reported to act as a tumor suppressor and was implicated in the chemosensitivity of numerous types of human malignancy.
The stable knockdown of PDCD4 in androgen-dependent prostate cancer cells enhanced subcutaneous tumor take rate <i>in vivo</i>, accelerated tumor growth, and was sufficient for castration-resistant tumor growth.
Recent evidence suggests that programmed cell death 4 (PDCD4), a novel tumor suppressor gene, inhibits tumor progression at transcriptional and translational levels and regulates multiple signal transduction pathways.
For example, miR-21, as a classic oncogene, was identified as the key regulator of PDCD4 by targeting its 3'-untranslated region (UTR) to promote tumor proliferation, migration, and invasion in colon, breast, and bladder carcinoma.
Furthermore, low PDCD4 <sup>TCs</sup> and high eIF4A1<sup>TCs</sup> predicted higher postoperative recurrence rate and are significant independent risk factors for early-stage OSCC.
Programmed cell death protein 4 (PDCD4) is a tumor suppressor gene that plays a role in cell apoptosis and DNA-damage response via interacting with eukaryotic initiation factor-4A (eIF4A) and P53.
Programmed cell death 4 (PDCD4) is a well-known tumor suppressor gene in several cancers, its post-transcriptional activity is directly controlled by miR-21, whose over-expression has been recently reported in MPM compared to normal mesothelium.
The results indicated that PDCD4 is associated with the histological grade of EEC, and that PDCD4 may be a valuable indicator of the degree of tumor malignancy in patients with EEC.
We found that activation of miRNA-21 and pSTAT3 were most pronounced following long-term arsenic exposure at low doses, and the effects on PDCD4 expression were most pronounced following short-term arsenic exposure at low doses. miRNA-21 inhibitors increased the expression of tumor suppressor genes PDCD4, PTEN, and Spry1 and miRNA-21-mimics suppressed the expression of these tumor suppressor genes.
Further studies on one such NAT, PDCD4-AS1 lncRNA reveal that it positively regulates the expression and activity of the tumor suppressor PDCD4 in mammary epithelial cells.
Programmed cell death 4 (PDCD4), a newly identified tumor suppressor, plays an important role in inhibiting tumorigenesis and tumor progression at the transcriptional and translational levels.
While the over-expression of tumor suppressor programmed cell death 4 (PDCD4) induces apoptosis, it was recently shown that PDCD4 knockdown also induced apoptosis.
It was observed that BCa cell proliferation and invasion and tumor growth were significantly inhibited, whereas apoptosis was enhanced in PDCD4-transfected cells treated with cisplatin compared with controls.
We also identified that the levels of 25 proteins were significantly associated with DTL overexpression in LuADCs, which include significant decreases in protein level of the tumor supressor genes such as PDCD4, NKX2-1 and PRKAA1.