Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in human breast cancer (BC) tumorigenesis. However, the mechanisms by which lncRNA and N⁶-methyladenosine (m⁶A) regulate BC tumorigenesis are still unclear. In the present research, LINC00958 was markedly overexpressed in BC tissue and cells, and LINC00958 upregulation promoted the tumor progression of BC cells. Mechanistically, m⁶A methyltransferase-like 3 (METTL3) gave rise to the upregulation of LINC00958 by promoting its RNA transcript stability. Moreover, LINC00958 acted as a competitive endogenous RNA for miR-378a-3p to promote YY1. Overall, these data provide novel insight into how m⁶A-mediated LINC00958 regulates BC tumorigenesis.

Increased resistance to apoptosis is a hallmark of many tumor cells. Survivin, a member of IAP family protein, is expressed in many human cancers and plays an important role in protecting cells fro...

Background: Abnormalities in mitochondrial structure or function are closely related to the development of malignant tumors. Mitochondrial metabolic reprogramming provides precursor substances and energy for the vital activities of tumor cells, so that cancer cells can rapidly adapt to the unfavorable environment of hypoxia and nutrient deficiency. Mitochondria can enable tumor cells to gain the ability to proliferate, escape immune responses, and develop drug resistance by altering constitutive junctions, oxidative phosphorylation, oxidative stress, and mitochondrial subcellular relocalization. This greatly reduces the rate of effective clinical control of tumors. Purpose: Explore the major role of mitochondria in cancer, as well as targeted mitochondrial therapies and mitochondria-associated markers. Conclusions: This review provides a comprehensive analysis of the various aspects of mitochondrial aberrations and addresses drugs that target mitochondrial therapy, providing a basis for clinical mitochondria-targeted anti-tumor therapy.

Giant cell tumors (GCTs) mainly occur in metaphyses of long bones and are generally considered histologically benign; however, GCTs may be locally aggressive with a high rate of local recurrence and exhibit the potential for distant metastasis. Primary GCT of the clivus is extremely rare and is easily misdiagnosed and, thus, treatment remains controversial. The present report describes the case of a 22‑year‑old male with GCT located in the skull base originating from the clivus, with the involvement of multiple cranial nerves, which was successfully treated with transnasal transsphenoidal surgery following adjuvant radiotherapy and intravenous bisphosphonate administration. The patient remains symptom free at two years of follow‑up. This report contributes to the limited literature regarding GCTs of the skull.