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MicroRNA 155 (miR-155) is an oncomir, generated as a noncoding RNA from the BIC gene whose promoter activity is mainly controlled via activation protein 1 (AP-1) and NF-κB transcription factors. We found that the expression levels of miR-155 and programmed cell death 4 (Pdcd4) exhibit inverse relationships in tongue cancer cells (SAS and AWL) and tumor tissues compared to their relationships in normal FBM cells and normal tongue tissues, respectively. In silico and in vitro studies with the 3′ untranslated region (UTR) of Pdcd4 via luciferase reporter assays, quantitative PCR (qPCR), and Western blotting showed that miR-155 directly targets Pdcd4 mRNA and blocks its expression. Ectopic expression of Pdcd4 or knockdown of miR-155 in tongue cancer cells predominantly reduces AP-1-dependent transcriptional activity of the BIC promoter and decreases miR-155 expression. In this study, we demonstrate that miR-155 expression is modulated by a feedback loop between Pdcd4, AP-1, and miR-155 which results in enhanced expression of miR-155 with a consequent progression of tongue tumorigenesis. Further, miR-155 knockdown increases apoptosis, arrests the cell cycle, regresses tumor size in xenograft nude mice, and reduces cell viability and colony formation in soft-agar and clonogenic assays. Thus, the restoration of Pdcd4 levels by the use of molecular manipulation such as using a miR-155 sponge has an essential role in the therapeutic intervention of cancers, including tongue cancer.

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JC Bose National Fellowship Grant SR/S2/JCB-28/2010 (to T. K. K.), and an Integrated Ph.D. program scholarship of Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR) (to S. S.). The authors declare that they have no conflicts of interest with the contents of this article. This article contains Figs. S1-S3, Files S1-S9, and Tables S1-S6. The RNA sequencing data reported in this paper have been submitted to the Gene Expression Omnibus (GEO) database under GEO accession no. GSE119654.

An experiment was carried out to investigate the bioefficacy of Emamectin benzoate against the larvae of Helicoverpa armigera and its natural enemies on chickpea at Breeding Seed Production Farm, JNKVV, Jabalpur, Madhya Pradesh, India, consecutively for two years during rabi season 2009 and 2010. The trial was laid out in Randomized Block Design with seven treatments and three replications. The pooled data of two years indicated that Emamectin benzoate 5% WG @ 9.4 and 8.1 g a.i. ha-1 were found to be most effective dose in reducing the H. armigera larval population and pod damage (1.28% and 1.29%, respectively) followed by Emamectin benzoate 5% WG @ 6.9 and 5.6 g a.i. ha-1 with 1.33 and 3.72% pod damage, respectively. The standard treatments of Chlorpyrifos 20% EC @ 500 g a.i. ha-1 and Ethion 50% EC @ 500 g a.i. ha-1 recorded 7.40% and 7.72% pod damage, respectively as compared to control plot (10.89% pod damage). All the treatments of Emamectin benzoate 5% WG did not show any adverse effects against Lady bird beetle and Chrysopa and no phytotoxic effects was observed on the chickpea crop. Seed yield was maximum (2260 kg ha-1) with the highest dose of Emamectin benzoate 5% WG @ 9.4 g a.i ha-1 followed by Emamectin benzoate 5% WG @ 8.1 and 6.9 g a.i ha-1 , respectively.