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The specificity protein (Sp) transcription factors (TFs) Sp1, Sp2, Sp3 and Sp4 exhibit structural and functional similarities in cancer cells and extensive studies of Sp1 show that it is a negative prognostic factor for patients with multiple tumor types. In this review, the role of Sp1, Sp3 and Sp4 in the development of cancer and their regulation of pro-oncogenic factors and pathways is reviewed. In addition, interactions with non-coding RNAs and the development of agents that target Sp transcription factors are also discussed. Studies on normal cell transformation into cancer cell lines show that this transformation process is accompanied by increased levels of Sp1 in most cell models, and in the transformation of muscle cells into rhabdomyosarcoma, both Sp1 and Sp3, but not Sp4, are increased. The pro-oncogenic functions of Sp1, Sp3 and Sp4 in cancer cell lines were studied in knockdown studies where silencing of each individual Sp TF decreased cancer growth, invasion and induced apoptosis. Silencing of an individual Sp TF was not compensated for by the other two and it was concluded that Sp1, Sp3 and Sp4 are examples of non-oncogene addicted genes. This conclusion was strengthened by the results of Sp TF interactions with non-coding microRNAs and long non-coding RNAs where Sp1 contributed to pro-oncogenic functions of Sp/non-coding RNAs. There are now many examples of anticancer agents and pharmaceuticals that induce downregulation/degradation of Sp1, Sp3 and Sp4, yet clinical applications of drugs specifically targeting Sp TFs are not being used. The application of agents targeting Sp TFs in combination therapies should be considered for their potential to enhance treatment efficacy and decrease toxic side effects. [ABSTRACT FROM AUTHOR]

Despite the recent advances in cancer therapy, cancer chemoresistance looms large along with radioresistance, a major challenge in dire need of thorough and minute investigation. Not long ago, cancer cells were reported to have proven refractory to the ferroptotic cell death, a newly discovered form of regulated cell death (RCD), conspicuous enough to draw attention from scholars in terms of targeting ferroptosis as a prospective therapeutic strategy. However, our knowledge concerning the underlying molecular mechanisms through which cancer cells gain immunity against ferroptosis is still in its infancy. Of late, the implication of non-coding RNAs (ncRNAs), including circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) in ferroptosis has been disclosed. Nevertheless, precisely explaining the molecular mechanisms behind the contribution of ncRNAs to cancer radio/chemotherapy resistance remains a challenge, requiring further clarification. In this review, we have presented the latest available information on the ways and means of regulating ferroptosis by ncRNAs. Moreover, we have provided important insights about targeting ncRNAs implicated in ferroptosis with the hope of opening up new horizons for overcoming cancer treatment modalities. Though a long path awaits until we make this ambitious dream come true, recent progress in gene therapy, including gene-editing technology will aid us to be optimistic that ncRNAs-based ferroptosis targeting would soon be on stream as a novel therapeutic strategy for treating cancer. [ABSTRACT FROM AUTHOR]

The quality of existing evidence about the impact of diet quality on colorectal cancer (CRC) risk has only rarely been assessed. In the current review, we searched PubMed, EMBASE, Web of Science, Cochrane, and the resulting references (up to January 2020) for studies that evaluated the role of high diet quality by extreme dietary index categorization and the risk of CRC. Two researchers independently performed the study selection, data extraction, and quality assessment. We then applied a random-effects meta-analysis to estimate the pooled odds ratios (ORs) and 95% confidence intervals (CIs) for CRC at the extremes of each dietary index, and we assessed the quality of the pooled results using the Grading of Recommendations Assessment, Development and Evaluation approach. A high diet quality was significantly associated with reduced CRC risk when patients had a low Diet Inflammatory Index score (OR, 0.66; 95%CI, 0.56–0.78), a high Mediterranean Diet Score (OR, 0.84; 95%CI, 0.78–0.90), high Dietary Approaches to Stop Hypertension adherence (OR, 0.83; 95%CI, 0.78–0.89), and a high Healthy Eating Index score (OR, 0.72; 95%CI, 0.64–0.80). The pooled results for all dietary indices were rated as being of low quality due to concerns over inconsistency or imprecision. We conclude that, despite a high diet quality appearing to have a preventive role in CRC, the evidence is currently of insufficient quality to develop dietary recommendations. [ABSTRACT FROM AUTHOR]