Journal of Medical Oncology and Therapeutics

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +441518081136

Mini Review - Journal of Medical Oncology and Therapeutics (2022) Volume 7, Issue 4

Molecular mechanisms of interaction between autophagy and digestion system in cancer.

Akemi Tanaka*

Department of Obstetrics and Gynaecology, Osaka University Graduate School of Medicine, Osaka, Japan

Corresponding Author:
Akemi Tanaka
Department of Obstetrics and Gynaecology
Osaka University Graduate School of Medicine
Osaka, Japan

Received: 25-June-2022, Manuscript No. JMOT-22-68748; Editor assigned: 01-July-2022, PreQC No. JMOT-22-68748(PQ); Reviewed: 14-July-2022, QC No. JMOT-22-68748; Revised: 19-July-2022, Manuscript No. JMOT-22-68748(R); Published: 25-July-2022, DOI: 10.35841/Jmot-7.4.117

Citation: Tanaka A. Molecular mechanisms of interaction between autophagy and digestion system in cancer. J Med Oncl Ther. 2022;7(4):117

Visit for more related articles at Journal of Medical Oncology and Therapeutics


Intriguingly, numerous highlights of the metastatic tumour cell, whether that be mesenchymal properties or capacity to elude safe reconnaissance, are related with a stem-like phenotype and linked to medicate resistance. Autophagy is upregulated in essential human breast, glioblastoma, melanoma, oesophageal cancer, and hepatocellular carcinoma upon movement to progressed metastatic disease and expression of autophagy markers in these cancers is related with destitute forecast, highlighting novel and imperative parts for autophagy at diverse focuses within the metastatic cascade.


Phenotype, Disease, Cancer, Autophagy, Carcinoma.


Here, we review later work characterizing modern capacities of autophagy in cancer metastasis counting how autophagy promotes procurement of promigratory and invasive properties, keeps up tumour cell stemless and drug resistant phenotypes, and moulds the coevolution of tumours with their microenvironment [1].

Autophagy contributes to the treatment resistance of numerous cancers, counting resistance to conventional genotoxic treatments, prostate cancer to androgen removal treatment, breast cancer to SERMs, Essence to Imagine, lung cancer to tyrosine kinase inhibitors, glioblastoma to temozolomide, myeloma to bortezomib, melanoma and brain cancers to B-Raff inhibitors, as well as resistance of different cancers to PI3K inhibitors. In this way, there's a compelling basis to combine these therapeutic approaches with specialists that repress autophagy, such as chloroquine, an antimalarial medicate that hinders autophagy by expanding the pH of the lysosome and blocking lysosomal proteases. Early clinical trials combining chloroquine with more routine treatments, such as temozolomide for glioblastoma treatment showed guarantee with autophagy hindrance more than doubling survival times [2].

Curcumin has anti-oxidant, anti-inflammatory and antiapoptotic exercises may be utilized on various diseases such as cardiovascular, and renal disease. In contract, curcumin too applies cytotoxic effects on different cells. Past studies showed that curcumin caused cytotoxic impacts on leukaemia cells through autophagy, apoptotic and pathways and S stage capture. In expansion, a study showed that curcumin moreover caused autophagy and apoptosis on pancreatic cancer cells whereas curcumin can cause G2/M stage capture but not S stage capture on pancreatic cancer cells. Nowadays us consider found that curcumin may initiate apoptosis and diminish G1 phase rate [3]. These ponders indicated curcumin-induced cytotoxic impacts may influence different cell cycle stage on diverse cell sorts.

The uremic poisons can be created from food digestion and digestion system. The amassing of uremic poisons can compound kidney work in chronic kidney malady patients. Indole sulphate (IS) and p-cresol sulfate (PCS), proteinbound organic compounds, are the foremost well-known uremic toxins in the world and both of them are not removed efficiently by haemodialysis [4]. The uremic toxins can actuate oxidative stretch and inflammation resulting in cell senescence and passing on renal tubular epithelial cells. In any case, the components of uremic toxins-induced cytotoxicity and the different cytotoxic impacts of IS and PCS stay to be studied. Many considers have illustrated protein-bound uremic poisons such as IS and PCS can actuate reactive oxygen species (ROS) generation coming about in oxidative stretch increment, and cause renal disease progression and vascular malady [5].

Adenocarcinoma and GEJ adenocarcinoma are presently combined into the same chapter since of their comparative histologic characteristics, chance components, and hereditary variations from the norm. Undifferentiated carcinoma of the oesophagus is presently considered a partitioned substance within the 5th edition,1 rather than being a subtype of squamous cell carcinoma (SCC) because it was within the past edition,2 because it needs any apparent separation (squamous, glandular, or neuroendocrine). This uncommon, understudied harm contains a destitute forecast. Esophageal squamous cell papilloma, a kind and more often than not coincidental injury not continuously caused by irresistible living beings, was not examined within the 4th edition2 and presently has its possess posting.


  1. Chaudhary S, Singh A, Kumar P, et al. Strategic targeting of non?small?cell lung cancer utilizing genetic material?based delivery platforms of nanotechnology. J Biochem Mol Toxicol. 2021;35(7):e22784.
  2. Indexed at, Google Scholar, Cross Ref

  3. Valentino F, Borra G, Allione P, et al. Emerging targets in advanced non-small-cell lung cancer. Future Oncol. 2018;14(13):61-72.
  4. Indexed at, Google Scholar, Cross Ref

  5. Schonewolf CA, Jolly S, Dess RT, et al. Particle Beam Therapy for Cardiac-Sparing Radiotherapy in Non-Small Cell Lung Cancer. Semin Radiat Oncol.2021.31(2):112-19.
  6. Indexed at, Google Scholar, Cross Ref

  7. Elias R, Morales J, Presley C, et al. Checkpoint inhibitors for non-small cell lung cancer among older adults. Curr Oncol Rep. 2017;19(9):1-9.
  8. Indexed at, Google Scholar, Cross Ref

  9. Pancewicz?Wojtkiewicz J. Epidermal growth factor receptor and notch signaling in non?small?cell lung cancer. Cancer Med. 2016;5(12):3572-8.
  10. Indexed at, Google Scholar, Cross Ref

Get the App