parkin KO reduces the development of lung tumors via cell cycle arrest by blocking the degradation of p21

H(2)O(2)-induced AP-1 activation and its effect on p21(WAF1/CIP1)-mediated G2/M arrest in a p53-deficient human lung cancer cell.

survivin can reduce the cell growth inhibition and apoptosis, and p53 elevates the p21 level, which may attenuate the cell death in the quercetin-treated human lung carcinoma cells

levels of p53/p21waf1 mRNA in blood lymphocytes collected before chemotherapy may predict the chemoresponses of lung cancer patients.

Results suggest that a combined analysis of three P21 polymorphisms might better predict the risk of lung cancer than the analysis of a single polymorphism.

the -KTS-containing variants of WT1 are directly involved in the regulation of p21(Waf1/Cip1) expression and the subsequent suppression of lymph node metastasis in human lung squamous cell carcinoma

p21 plays a role in lung cancer drug-resistance process

the reduction of p21 protein levels plays an essential role in early-stage human papillomavirus-associated lung tumorigenesis and is correlated with poor relapse free survival

Loss of p21 expression was frequently observed in lung cancers and malignant pleural mesotheliomas and aberrant methylation was one of the mechanisms of suppression of p21.

based on our meta-analysis, p21 Ser31Arg polymorphism does not appear to act as an independent lung cancer risk factor

FoxM1, p27(kip1) and p21(waf1/cip1) showed distinct immunoreactivity according to histological subtype, which may help in the differential diagnosis of pulmonary neuroendocrine tumours.

upregulation of HOTAIR contributes to the cisplatin resistance of lung adenocarcinoma cells, at least in part, through the regulation of p21 expression.

Following upregulation, PRP19 repressed cell proliferation and tumor growth by upregulating the expression of the cell cycle arrest protein p21 in lung carcinoma tissues.

p53, KLF4, and p21 showed altered expression patterns in pulmonary neuroendocrine neoplasms. Lack of KLF4 and p21 expression was associated with accumulation of aggressive features in typical carcinoids.

Cigarette smoking and overexpression of p53 or p21 are associated with poor prognosis in non-small cell lung cancer.

Results show that lncRNA ANRIL plays a key role in non-small cell lung cancer (NSCLC) development by associating its expression with survival in patients with NSCLC through silencing of KLF2 and P21 transcription.

Study provides evidence that miR-208a can affect the proliferation and radio-sensitivity of human lung cancer cells by targeting p21.

p21 is a bona fide ubiquitylation substrate for CHIP.p21 role in lung cancer radioresistance.

The expression of p53 fulllength transcript and Delta133p53 isoforms alpha, beta and gamma transcripts, MDM2 and p21 transcripts were determined by reverse transcriptionquantitative polymerase chain reaction, in total RNA isolated from 17 lung carcinoma specimens and 17 corresponding adjacent noncancerous tissues.

PKCzeta was specifically involved in ACOT7 depletion-mediated cell cycle arrest as an upstream molecule of the p53-p21 signaling pathway in MCF7 human breast carcinoma and A549 human lung carcinoma cells.

Overexpression of these two microRNAs in A549 induced cell-cycle arrest and cell senescence, delayed cell proliferation and colony formation, and inhibited migration and invasion. In conclusion, microRNA-mediated RNAa depends on the cell context, and miR-1236 and miR-370 can inhibit non-small-cell lung carcinoma cell growth by upregulating p21 expression in vitro

It is a pathogenetic factor for non-small cell lung cancer and its signaling pathway is modulated by gefitinib.

rescue experiments indicated that SNHG20 functioned as an oncogene partly via repressing p21 in non-small cell lung cancer (NSCLC) cells. Taken together, our findings demonstrate that SNHG20 is a new candidate for use in NSCLC diagnosis, prognosis and therapy.

AFAP1-AS1 epigenetically silences p21 transcription by binding to EZH2 thus promoting non-small cell lung cancer cell growth.

These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)

maintaining p21 expression can result in increased interactions between p21 and PCNA or CDK2, resulting in cell cycle arrest, which ultimately inhibits lung tumor growth

Low CIP1 expression is associated with non-small cell lung cancer.

MiR-509-3-5p-NONHSAT112228.2 Axis Regulates p21 and Suppresses Proliferation and Migration of lung cancer Cells.

CDKN1A upregulation and cisplatinpemetrexed resistance in nonsmall cell lung cancer cells.

[Role of P21 in Resistance of lung cancer].