Imran Khan

Dr. Imran Khan

Department of Nebraska Medical Center, University of Nebraska Medical Center, Omaha, Nebraska, USA
orcid

Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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5 September 2017 in Nutrition and Cancer
Verified
Journal Article
Closed access
FKFahad Khan
Fahad Khan
Imran KhanImran Khan
Imran Khan
AFArshi Farooqui
Arshi Farooqui
IAIrfan A. Ansari
Irfan A. Ansari
Carvacrol, a major monoterpenoid phenol from Origanum and Thymus species, has been shown to exhibit antiproliferative and anticancer properties in a few recent studies. Nevertheless, detailed mechanism of the action of this compound in prostate cancer has not been elucidated yet. Therefore, in the current study, we examined the anticancer activity and mechanism of the action of carvacrol against human prostate cancer cells. It was found that the treatment of DU145 cells with carvacrol decreased cell viability in a concentration and time-dependent manner. The antiproliferative action of carvacrol leads to induction of apoptosis as confirmed by nuclear condensation, Annexin V-FITC/PI positive cells, and caspase-3 activation. In addition, carvacrol augmented reactive oxygen species generation and disruption in the mitochondrial membrane potential which has not been reported in the previous studies of carvacrol with prostate cancer. Moreover, carvacrol-induced apoptosis of prostate cancer cells was also accompanied by significant amount of growth arrest at the G0/G1 phase of the cell cycle which has also not been documented previously. To sum up, this study has established that carvacrol could be a promising chemotherapeutic agent and could have a direct practical implication and translational relevance to prostate cancer patients as Origanum consumption may retard prostate cancer progression.

1 July 2017 in Free Radical Biology and Medicine
Verified
Journal Article
Closed access
Sahir Sultan AlviSahir Sultan Alvi
Sahir Sultan Alvi
IAIrfan A. Ansari
Irfan A. Ansari
Imran KhanImran Khan
Imran Khan
JIJohar Iqbal
Johar Iqbal
MKM. Salman Khan
M. Salman Khan

21 May 2018 in Nutrition and Cancer
Verified
Journal Article
Closed access
Imran KhanImran Khan
Imran Khan
FKFahad Khan
Fahad Khan
AFArshi Farooqui
Arshi Farooqui
IAIrfan Ahmad
Irfan Ahmad
Andrographolide, a diterpenoid lactone and a major constituent of Andrographis paniculata Nees, exhibits remarkable anticancer activity. However, the effect of andrographolide on colon cancer has not been completely elucidated yet. Thus, we investigated the chemopreventive potential of andrographolide in colon cancer HT-29 cells. The cytotoxic potential of andrographolide on HT-29 cells was determined by MTT assay, trypan blue exclusion assay, colony formation assay, and morphological analysis; and apoptotic property by DAPI and Hoechst staining, FITC-Annexin V assay, DNA fragmentation assay and caspase-3 activity assay. To elucidate andrographolide action, intracellular reactive oxygen species (ROS) level was determined by DCFDA dye; change in mitochondrial potential by Rhodamine123 and Mito Tracker Red CMXRos dye; and cell cycle modulatory property by flow cytometric analysis. Results of the study have shown that andrographolide decreased cell viability of HT-29 cells in a dose- and time-dependent manner. Furthermore, andrographolide induced apoptosis in HT-29 cells which seemed to be linked with augmented intracellular ROS level and disruption of mitochondrial membrane potential. Interestingly, andrographolide caused significant cell cycle arrest in G2/M phase at lower doses, but, in G0/G1 phase at higher doses. In summary, our results indicated that andrographolide exhibited antiproliferative and apoptotic properties against colon cancer HT-29 cells.

1 January 2018 in Biomedicine & Pharmacotherapy
Verified
Journal Article
Open access
AFArshi Farooqui
Arshi Farooqui
FKFahad Khan
Fahad Khan
Imran KhanImran Khan
Imran Khan
IAIrfan Ahmad
Irfan Ahmad
Cervical cancer is the fourth most common cancer among women worldwide and is a major cause of morbidity and mortality. High-risk Human Papilloma Virus (mostly type 16 & 18) infection is the primary risk factor for the development of cervical carcinoma. The quest for strong, safe and cost effective natural antiproliferative agents that could reduce cervical cancer have been focussed now a day. Recently, glycyrrhizin, a triterpene glycoside (saponin) from licorice (Glycyrrhiza glabra Linn.), has been shown to exhibit potent antiproliferative and anticancer properties in a few preliminary studies. However, potential of this compound in cervical cancer has not been elucidated yet. Therefore the objective of this study was to analyze the antiproliferative and apoptotic properties of glycyrrhizin in human cervical cancer HeLa cells. Our results showed that glycyrrhizin exposure significantly reduced the cell viability of HeLa cells with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. The intracellular ROS generation assay showed dose-related increment in ROS production induced by glycyrrhizin. Glycyrrhizin also induced apoptosis in cervical cancer cells by exerting mitochondrial depolarization. Cell cycle study showed that glycyrrhizin induced cell cycle arrest in G0/G1 phase of cell cycle in a dose dependent manner. Thus, this study confirms the efficacy of glycyrrhizin in cervical cancer cells which could be an adjunct in the better prevention and management of cervical cancer worldwide.

1 December 2017 in Colloids and Surfaces B: Biointerfaces
Verified
Journal Article
Closed access
SISana Iram
Sana Iram
MZManaal Zahera
Manaal Zahera
SKSalman Khan
Salman Khan
Imran KhanImran Khan
Imran Khan
ASAsad Syed
Asad Syed
MKMohd Sajid Khan
Mohd Sajid Khan

Verified
Journal Article
Open access
PDF file
Imran KhanImran Khan
Imran Khan
MBMohammad Hassan Baig
Mohammad Hassan Baig
SMSadaf Mahfooz
Sadaf Mahfooz
MRMoniba Rahim
Moniba Rahim
BKBusra Karacam
Busra Karacam
MHMustafa Aziz Hatiboglu
Mustafa Aziz Hatiboglu
Autophagy is a process essential for cellular energy consumption, survival, and defense mechanisms. The role of autophagy in several types of human cancers has been explicitly explained; however, the underlying molecular mechanism of autophagy in glioblastoma remains ambiguous. Autophagy is thought to be a “double-edged sword”, and its effect on tumorigenesis varies with cell type. On the other hand, autophagy may play a significant role in the resistance mechanisms against various therapies. Therefore, it is of the utmost importance to gain insight into the molecular mechanisms deriving the autophagy-mediated therapeutic resistance and designing improved treatment strategies for glioblastoma. In this review, we discuss autophagy mechanisms, specifically its pro-survival and growth-suppressing mechanisms in glioblastomas. In addition, we try to shed some light on the autophagy-mediated activation of the cellular mechanisms supporting radioresistance and chemoresistance in glioblastoma. This review also highlights autophagy’s involvement in glioma stem cell behavior, underlining its role as a potential molecular target for therapeutic interventions.