This aim of the present study was to identify the relationship between hesperidin and microRNA (miR)‑132, and to study the role of hesperidin and miR‑132 in the pathogenesis of non‑small cell lung cancer (NSCLC). Computational analysis and luciferase assays were performed to identify the target of miR‑132. Subsequently, reverse transcription‑quantitative PCR and western blot assays were used to detect the effect of miR‑132 and hesperidin on the expression of haematological and neurological expressed 1 (HN1) and zinc finger E‑box binding homeobox 2 (ZEB2). Finally, MTT assays and flow cytometry analysis were used to investigate the effect of hesperidin on cell proliferation and apoptosis. ZEB2 was identified as a target gene of miR‑132, and transfection with miR‑132 mimic reduced the luciferase activity of the wild‑type ZEB2 3’‑untranslated region (3’‑UTR) but not that of the mutant ZEB2 3’‑UTR. By contrast, neither transfection with miR‑132 mimic nor hesperidin treatment affected HN1 expression. Furthermore, hesperidin evidently inhibited cell proliferation and promoted apoptosis in a dose‑dependent manner. Furthermore, the tumour volume in rats transplanted with NSCLC cells and treated with hesperidin was notably smaller compared with that in rats transplanted with NSCLC cells alone, while treatment with hesperidin significantly reduced the colony formation efficiency of NSCLC cells by increasing miR‑132 expression and decreasing ZEB2 expression. To the best of our knowledge, the present study demonstrated for the first time that the administration of hesperidin decreased the expression of ZEB2 by upregulating the expression of miR‑132, which in turn promoted apoptosis and inhibited the proliferation of NSCLC cells.Osteosarcoma is the most common primary malignant tumor of the bone in adolescents and children, with high rates of metastasis and a poor prognosis. Recently, osteosarcoma cancer stem/stem‑like cells (CSCs) have been identified as the main cause of recurrence and metastasis. Stress‑induced phosphoprotein 1 (STIP1), a co‑chaperone that binds to heat shock proteins 70 and 90, is abnormally expressed in several tumor cell lines, and may play an important role in tumor cell migration and invasion. These features indicate that STIP1 may represent a new therapeutic target for osteosarcoma CSCs. However, the role of STIP1 in osteosarcoma CSC migration and invasion remains largely unknown. In the present study, CD133‑positive osteosarcoma CSCs were first isolated and cultured by magnetic cell sorting and serum‑free medium suspension cell sphere culture, respectively. check details of STIP1 by small interfering RNA significantly was then shown to inhibit the migration and invasion of these cells, possibly due to the regulation of the expression of matrix metalloproteinase (MMP)‑2, MMP‑9 and tissue inhibitor of metalloproteinase‑2. Furthermore, data from the present study suggested that the knockdown of STIP1 decreased the levels of phosphorylated Akt and phosphorylated ERK1/2. In summary, these findings indicate that targeting STIP1 in osteosarcoma may constitute a viable molecular targeted therapy strategy for the inhibition of CSC invasion and migration.The erythroid differentiation regulator 1 (Erdr1) protein has been studied for its role in various inflammatory skin diseases, including skin cancer, actinic keratosis and psoriasis. However, the therapeutic effects of Erdr1 on wound repair and its underlying mechanisms remain unknown. The present study aimed to investigate the effects of Erdr1 on wound healing in vitro and in vivo. #link# The results demonstrated that treatment with recombinant Erdr1 enhanced wound healing in vivo and in vitro. In addition, Erdr1 increased the proliferation and migration of human dermal fibroblasts (HDFs). Notably, Erdr1 significantly induced the production of the chemoattractant C‑C motif chemokine ligand 2 (CCL2) and recruited immune cells involved in wound healing. Treatment with recombinant Erdr1 induced the activation of the ERK1/1, p38 and JNK1/2 mitogen‑activated protein (MAP) kinases. Treatment with specific inhibitors for MAP kinase inhibitors markedly suppressed cell proliferation and migration, and inhibited the production of CCL2 in HDFs. Furthermore, the inhibition of CCL2 with a neutralizing antibody significantly suppressed the recombinant Erdr1‑induced proliferation and migration of HDFs. The wound healing activity of Erdr1 was comparable to that of epidermal growth factor. Taken together, these results demonstrated that Erdr1 promoted the proliferation and migration of HDFs and exhibited potent wound healing properties mediated by CCL2. Therefore, the results of the present study suggested that Erdr1 may be a potential therapeutic target for promoting wound healing.Arsenic is a well‑documented environmental toxicant that can induce neurotoxicity and peripheral vascular diseases. In fact, arsenic trioxide has been used to treat various cancer types. Oral cancer has been in the top ten common cancers for decades in Taiwan, and the incidence rate is continuously increasing. The majority of oral cancers are associated with excessive tobacco, alcohol consumption and betel chewing. To the best of our knowledge, no study has revealed the effect of arsenic compounds on oral cancers. Thus, the present study used OEC‑M1 oral squamous carcinoma cells treated with sodium arsenite (NaAsO2) and dimethylarsenic acid (DMA) to determine whether both arsenic compounds could exert anticancer effects on oral cancer. The results demonstrated that NaAsO2 and DMA induced rounding up and membrane blebbing in OEC‑M1 cells, which are morphological characteristics of apoptosis. Annexin V/PI double staining analysis further confirmed that both arsenic compounds induced apoptosis of OEC‑M1 cells. In addition, NaAsO2 and DMA significantly decreased the survival rate and increased the percentage of OEC‑M1 cells in the subG1 and G2/M phases (P less then 0.05). Furthermore, both arsenic compounds significantly activated the cleavage of caspase‑8, ‑9, ‑3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC‑M1 cells (P less then 0.05). Collectively, the findings of the present study indicated that NaAsO2 and DMA stimulate extrinsic and intrinsic apoptotic pathways through the activation of the MAPK pathways to induce apoptosis of OEC‑M1 cells, suggesting that NaAsO2 and DMA may be used as novel anticancer drugs for oral cancers.