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Autophagy is an evolutionarily conserved process that plays a role in regulating homeostasis under physiological conditions. However, dysregulation of autophagy is observed in the development of human diseases, especially cancer. Autophagy has reciprocal functions in cancer and may be responsible for either survival or death. Hepatocellular carcinoma (HCC) is one of the most lethal and common malignancies of the liver, and smoking, infection, and alcohol consumption can lead to its development. Genetic mutations and alterations in molecular processes can exacerbate the progression of HCC. The function of autophagy in HCC is controversial and may be both tumor suppressive and tumor promoting. Activation of autophagy may affect apoptosis in HCC and is a regulator of proliferation and glucose metabolism. Induction of autophagy may promote tumor metastasis via induction of EMT. In addition, autophagy is a regulator of stem cell formation in HCC, and pro-survival autophagy leads to cancer cell resistance to chemotherapy and radiotherapy. Targeting autophagy impairs growth and metastasis in HCC and improves tumor cell response to therapy. Of note, a large number of signaling pathways such as STAT3, Wnt, miRNAs, lncRNAs, and circRNAs regulate autophagy in HCC. Moreover, regulation of autophagy (induction or inhibition) by antitumor agents could be suggested for effective treatment of HCC. In this paper, we comprehensively review the role and mechanisms of autophagy in HCC and discuss the potential benefit of targeting this process in the treatment of the cancer. Graphical abstract

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Tadalafil has positive effects on neurodevelopment and antioxidant defense system, but there is no information for its possible role during gestation on reflexive motor behavior in offspring. So current study determined the effect of prenatal exposure to the Tadalafil on reflexive motor behaviors and antioxidant activity in mice offspring and antidepressive behaviors in postpartum dams. Forty pregnant female NMRI mice were allocated into four groups. In control group, mice received water while in Groups 2-4, female mice orally gavage with Tadalafil (0.4, 0.8, and 1.6 mg/kg) at gestation day (GD) 5, 8, 11, 14, and 17, respectively. Following delivery, pups were selected and reflexive motor behaviors determined using ambulation, hind-limb foot angle, surface righting, hind-limb strength, grip strength, front-limb suspension, and negative geotaxis tests. Also, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant status (TAS) were determined in offspring. On Day 2 postpartum, antidepressant activity of Tadalafil was determined by open field test (OFT), rotarod, forced swimming test (FST), and tail suspension test (TST) in dams. Based on the findings, maternal exposure to Tadalafil improved ambulation score, hind-limb suspension score, grip strength, and front-limb suspension in offspring (P < 0.05).Prenatal exposure to Tadalafil decreased surface righting, hind-limb foot angle, and negative geotaxis in offspring (P < 0.05). Tadalafil decreased blood MDA and increased SOD and GPx levels in offspring (P < 0.05). Tadalafil significantly decreased immobility time in FST and TST and increased number of squares crossed in OFT and spending time on rotarod on postpartum mice (P < 0.05). These results suggested that parental exposure of Tadalafil has positive effect on reflexive motor and postpartum behaviors.