MiRNAs are single-stranded small RNAs that do not encode proteins. They can combine complementarily with the 3’-UTRs of target gene mRNA molecules to promote targeted mRNA degradation or inhibit mRNA translation, thereby regulating gene expression at the post-transcriptional level. MiRNAs participate in regulation of cell cycling, growth, apoptosis, differentiation, and stress responses. MiRNA-145 (miR-145) is a tumor suppressor that targets various tumor-specific genes and proteins, thereby influencing related signaling pathways. MiR-145 not only regulates tumor growth, invasion, and metastasis, but is also important for tumor angiogenesis and tumor stem cell proliferation. Here, we review the roles and mechanisms of miR-145 in the diagnosis and treatment of malignant tumors. Published data confirm that miR-145 expression in various tumors is significantly lower than that in normal tissues and that overexpression of miR-145 inhibits the growth of different tumor cells, significantly reduces the ability of tumors to spread, and improves sensitivity to chemotherapeutic drugs. We conclude that miR-145 is a potential marker for use in the early diagnosis and prognostic evaluation of patients with cancer, has a role as a tumor suppressor, and is a promising cancer treatment target candidate.

Head-and-neck cancer is a major form of the disease worldwide. Treatment consists of surgery, radiation therapy and chemotherapy, but these have not resulted in improved survival rates over the past few decades. Versatile nanoparticles, with selective tumor targeting, are considered to have the potential to improve these poor outcomes. Application of nanoparticle-based targeted therapeutics has extended into many areas, including gene silencing, chemotherapeutic drug delivery, radiosensitization, photothermal therapy, and has shown much promise. In this review, we discuss recent advances in the field of nanoparticle-mediated targeted therapeutics for head-and-neck cancer, with an emphasis on the description of targeting points, including future perspectives.

Hypoxic resistance is the main obstacle to radiotherapy for laryngeal carcinoma. Our previous study indicated that hypoxia‐inducible factor 1α (HIF‐1α) and glucose transporter 1 (Glut‐1) double knockout reduced tumour biological behaviour in laryngeal carcinoma cells. However, their radioresistance mechanism remains unclear. In this study, cell viability was determined by CCK8 assay. Glucose uptake capability was evaluated by measurement of ¹⁸F‐fluorodeoxyglucose radioactivity. A tumour xenograft model was established by subcutaneous injection of Tu212 cells. Tumour histopathology was determined by haematoxylin and eosin staining, immunohistochemical staining, and TUNEL assays. Signalling transduction was evaluated by Western blotting. We found that hypoxia induced radioresistance in Tu212 cells accompanied by increased glucose uptake capability and activation of the PI3K/Akt/mTOR pathway. Inhibition of PI3K/Akt/mTOR activity abolished hypoxia‐induced radioresistance and glucose absorption. Mechanistic analysis revealed that hypoxia promoted higher expressions of HIF‐1α and Glut‐1. Moreover, the PI3K/Akt/mTOR pathway was a positive mediator of HIF‐1α and/or Glut‐1 in the presence of irradiation. HIF‐1α and/or Glut‐1 knockout significantly reduced cell viability, glucose uptake and PI3K/Akt/mTOR activity, all of which were induced by hypoxia in the presence of irradiation. In vivo analysis showed that knockout of HIF‐1α and/or Glut‐1 also inhibited tumour growth by promoting cell apoptosis, more robustly compared with the PI3K inhibitor wortmannin, particularly in tumours with knockout of both HIF‐1α and Glut‐1. HIF‐1α and/or Glut‐1 knockout also abrogated PI3K/Akt/mTOR signalling transduction in tumour tissues, in a manner similar to wortmannin. HIF‐1α and/or Glut‐1 knockout facilitated radiosensitivity in laryngeal carcinoma Tu212 cells by regulation of the PI3K/Akt/mTOR pathway.

Objective: Magnetic resonance imaging (MRI) provides important information regarding tumors in the parapharyngeal space (PPS), revealing their origin, whether they are benign or malignant, and their relationships with surrounding structures. Methods: Twelve tumors in the PPS were completely excised using an endoscopically assisted transoral approach (EATA). The MRI features were analyzed. Results: Ten pleomorphic adenomas confirmed on postoperative pathological examination had the parotid pedicle sign. A fat space between the tumor and parotid gland may distinguish such a tumor from a tumor arising from a minor salivary gland in the prestyloid space and a tumor arising from the deep lobe of the parotid gland. Both the jugular vein and carotid artery were displaced posteriorly in all 10 cases of pleomorphic adenomas. The principal features of the two schwannomas confirmed on postoperative pathological examination were separation of the internal carotid artery and internal jugular vein and anteromedial displacement of the internal carotid artery, suggesting that the tumors originated in the poststyloid space. In this review, 95 tumors were excised by the EATA in the English-language literature. Conclusions: MRI renders differential diagnosis possible. PPS tumors may be completely excised via an EATA guided by tumor features evident on preoperative MRI.

Beclin 1, a positive regulator of autophagy, behaves as a double-edged sword in tumorigenesis. Beclin 1 contributes to tumor suppression by removing defective or damaged organelles and other cellular components; however, its activity can also stimulate cancer initiation and progression. In head and neck cancer, Beclin 1 overexpression promotes autophagy, which limits DNA damage and chromosomal instability and increases necrosis and inflammation by impacting apoptotic and autophagic pathways. This paper reviews the relationship between Beclin 1, carcinogenesis and head and neck cancer prognosis.